Interaction of the endocrine system with inflammation: a function of energy and volume regulation
Open accessAbstract
During acute systemic infectious disease, precisely regulated release of energy-rich substrates (glucose, free fatty acids, and amino acids) and auxiliary elements such as calcium/phosphorus from storage sites (fat tissue, muscle, liver, and bone) are highly important because these factors are needed by an energy-consuming immune system in a situation with little or no food/water intake (sickness behavior). This positively selected program for short-lived infectious diseases is similarly applied during chronic inflammatory diseases. This review presents the interaction of hormones and inflammation by focusing on energy storage/expenditure and volume regulation. Energy storage hormones are represented by insulin (glucose/lipid storage and growth-related processes), insulin-like growth factor-1 (IGF-1) (muscle and bone growth), androgens (muscle and bone growth), vitamin D (bone growth), and osteocalcin (bone growth, support of insulin, and testosterone). Energy expenditure hormones are represented by cortisol (breakdown of liver glycogen/adipose tissue triglycerides/muscle protein, and gluconeogenesis; water retention), noradrenaline/adrenaline (breakdown of liver glycogen/adipose tissue triglycerides, and gluconeogenesis; water retention), growth hormone (glucogenic, lipolytic; has also growth-related aspects; water retention), thyroid gland hormones (increase metabolic effects of adrenaline/noradrenaline), and angiotensin II (induce insulin resistance and retain water). In chronic inflammatory diseases, a preponderance of energy expenditure pathways is switched on, leading to typical hormonal changes such as insulin/IGF-1 resistance, hypoandrogenemia, hypovitaminosis D, mild hypercortisolemia, and increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Though necessary during acute inflammation in the context of systemic infection or trauma, these long-standing changes contribute to increased mortality in chronic inflammatory diseases.
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Written from the paper’s full text.
TL;DR
This review proposes that neuroendocrine changes in chronic inflammatory diseases reflect an evolutionarily selected energy re-allocation program: energy storage hormones are suppressed while energy expenditure hormones are activated to supply an activated immune system. Long-term use of this acute-inflammatory program contributes to insulin resistance, cachexia, osteoporosis, and volume overload/hypertension, increasing morbidity and mortality in chronic inflammatory diseases.
Key findings
- The review frames three major energy consumers—brain, muscle, and immune system—as each using approximately 2,000 kJ/day under resting conditions; immune system expenditure is estimated at 1,600 kJ/day plus 400 kJ/day for growth-related phenomena in adults. Storage organs in an 85-kg person are given as liver 2,500 kJ as glycogen, muscle 50,000 kJ as degradable protein, and fat tissue 500,000 kJ as triglycerides; total storage is approximately 560,000 kJ, with 10,000 kJ/day needed in a sedentary lifestyle.
- In chronic inflammatory diseases, the paper reports a preponderance of energy expenditure pathways, with typical changes including insulin/IGF-1 resistance, hypoandrogenemia, hypovitaminosis D, mild hypercortisolemia, and increased activity of the sympathetic nervous system and renin-angiotensin-aldosterone system. These changes are proposed to support allocation of energy-rich fuels and calcium/phosphorus to the activated immune system but, long term, lead to cachexia, osteoporosis, insulin resistance, and volume overload/hypertension.
- Energy storage hormones are listed as insulin, IGF-1, androgens, estrogens (bi-modal), vitamin D, osteocalcin, and the vagus nerve; energy expenditure hormones are cortisol, noradrenaline/adrenaline, growth hormone, thyroid hormones, and angiotensin II. Table 2 summarizes their immune effects, observed changes in chronic inflammatory rheumatic diseases, and long-term consequences.
- Chronic smoldering inflammation is described as established when serum IL-6 rises from normal levels of 1 pg/mL to approximately 10 to 100 pg/mL, which can increase resting metabolic rate; slightly elevated C-reactive protein is also linked to insulin resistance as part of the energy re-allocation program.
Methods
- Narrative review, not a primary study; it synthesizes prior literature on endocrine-immune interactions, energy storage/expenditure, and volume regulation, using an evolutionary-medicine framework.
- No new sample or dataset is analyzed. The paper organizes evidence into conceptual figures and two summary tables: Table 1 covers hormone effects on fat tissue, muscle, liver, bone, and kidneys; Table 2 covers immune/inflammatory effects, observed changes in chronic inflammatory rheumatic diseases, and long-term consequences.
- Main analysis is qualitative and interpretive, drawing on cited animal and human studies rather than systematic review, meta-analysis, or formal evidence grading.
Limitations
- The paper states that no treatment schemes exist to treat the individual abnormalities in chronic inflammatory diseases and that the next decade should address treatment rules because these complications determine advanced mortality. It also notes that experimental proof is necessary in the complex growth hormone–IGF-1 system, that few human studies have addressed serum RAAS hormones in rheumatic diseases, that osteocalcin results are little and ambiguous, that thyroid mechanisms remain enigmatic, and that local deiodinase expression has not been tested in adipose tissue during inflammation.
- Evident from the text: this is a narrative review without a systematic search strategy or formal quality assessment, and many conclusions are mechanistic or hypothetical, relying on animal models, small human studies, or indirect associations rather than primary causal testing.
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Claims the paper makes
0 of 130 cited sources checked · 0 supported · 0 flagged
- Findingcitation
Brain, muscle, and immune system use similar amounts of energy-rich fuels.
“The platform of the theory is based on the fact that brain, muscle, and immune system use similar amounts of energy-rich fuels (Figure 1).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [4] Straub RH, Cutolo M, Buttgereit F, Pongratz G: Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J Intern Med. 2010, 267: 543-560. source
Not checked in the free run.
- Findingcitation
Slightly elevated serum levels of C-reactive protein (IL-6-dependent) are closely interrelated with insulin resistance.
“This is confirmed by studies that describe a close interrelation of slightly elevated serum levels of C-reactive protein (IL-6-dependent) and a key element of the energy re-allocation program, namely insulin resistance [9,10].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [9] Hak AE, Stehouwer CD, Bots ML, Polderman KH, Schalkwijk CG, Westendorp IC, Hofman A, Witteman JC: Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women. Arterioscler Thromb Vasc Biol. 1999, 19: 1986-1991. source
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- cites [10] Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW: C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue?. Arterioscler Thromb Vasc Biol. 1999, 19: 972-978. source
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- Interpretationreasoning
These long-standing changes contribute to increased mortality in chronic inflammatory diseases.
“Though necessary during acute inflammation in the context of systemic infection or trauma, these long-standing changes contribute to increased mortality in chronic inflammatory diseases.”
Quote in the paperNot a substantial claim - Premisecitation
Energy-rich fuel allocation is important for an activated immune system.
“(i) energy-rich fuel allocation is important for an activated immune system [4,5]”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [4] Straub RH, Cutolo M, Buttgereit F, Pongratz G: Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J Intern Med. 2010, 267: 543-560. source
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- cites [5] Spies CM, Straub RH, Buttgereit F: Energy metabolism and rheumatic diseases: from cell to organism. Arthritis Res Ther. 2012, 14: 216-225. source
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- Premisecitation
Insulin is the major hormone responsible for uptake of energy-rich substrates into liver, muscle, and adipose tissue when there is no insulin resistance.
“Insulin is the major hormone responsible for uptake of energy-rich substrates into liver, muscle, and adipose tissue when there is no insulin resistance.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [12] Taubes G: Treat obesity as physiology, not physics. Nature. 2012, 492: 155- source
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- Interpretationreasoning
The activated immune system is the independent stimulus of the observed endocrine and neuronal changes in inflammation as part of an energy re-allocation program.
“The theory says that the activated immune system is the independent stimulus of the observed endocrine and neuronal changes in inflammation as part of an energy re-allocation program.”
Quote in the paperNot a substantial claim - Interpretationreasoning
Precise regulation of energy-rich fuel allocation to brain, muscle, and immune system is necessitated by their similar energy use.
“This circumstance necessitates precise regulation of energy-rich fuel allocation to these three systems (Figure 2).”
Quote in the paperSubstantial claim - Premisecitation
Increased activity of the water retention system accompanies energy allocation to the immune system.
“(ii) increased activity of the water retention system accompanies energy allocation to the immune system [6]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [6] Straub RH: Evolutionary medicine and chronic inflammatory state - known and new concepts in pathophysiology. J Mol Med. 2012, 90: 523-534. source
Not checked in the free run.
- Premisereasoning
During acute systemic infectious disease, precisely regulated release of energy-rich substrates (glucose, free fatty acids, and amino acids) and auxiliary elements such as calcium/phosphorus from storage sites is highly important because these factors are needed by an energy-consuming immune system in a situation with little or no food/water intake.
“During acute systemic infectious disease, precisely regulated release of energy-rich substrates (glucose, free fatty acids, and amino acids) and auxiliary elements such as calcium/phosphorus from storage sites (fat tissue, muscle, liver, and bone) are highly important because these factors are needed by an energy-consuming immune system in a situation with little or no food/water intake (sickness”
Quote in the paperSubstantial claim - Interpretationcitation
An observable increase of inflammatory cytokines at relatively low serum levels can induce a re-allocation program of energy-rich fuels directed toward the activated immune system.
“The observable increase of inflammatory cytokines at relatively low serum levels can induce a re-allocation program of energy-rich fuels directed toward the activated immune system.”
Quote in the paperSubstantial claim - Interpretationreasoning
The positively selected program for short-lived infectious diseases is similarly applied during chronic inflammatory diseases.
“This positively selected program for short-lived infectious diseases is similarly applied during chronic inflammatory diseases.”
Quote in the paperNot a substantial claim - Premisenone given
Energy expenditure hormones are typically released upon stressful events such as hypoglycemia or other forms of stress such as acute inflammation or trauma.
“Energy expenditure hormones are typically released upon stressful events such as hypoglycemia or other forms of stress such as acute inflammation or trauma.”
Quote in the paperNot a substantial claim - Interpretationnone given
Similar energy re-allocation programs are used in chronic inflammatory diseases.
“Similar programs are used in CIDs.”
Quote in the paperNot a substantial claim - Interpretationcitation
Growth hormone in contrast to IGF-1 has many catabolic effects leading to provision of energy-rich substrates to an activated immune system in inflammation.
“Thus, growth hormone in contrast to IGF-1 has many catabolic effects leading to provision of energy-rich substrates to an activated immune system in inflammation.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] LeRoith D, Yakar S: Mechanisms of disease: metabolic effects of growth hormone and insulin-like growth factor 1. Nat Clin Pract Endocrinol Metab. 2007, 3: 302-310. source
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- Premisecitation
IGF-1 has mainly pro-inflammatory effects.
“IGF-1 was demonstrated to have mainly pro-inflammatory effects [83,84].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [83] Heemskerk VH, Daemen MA, Buurman WA: Insulin-like growth factor-1 (IGF-1) and growth hormone (GH) in immunity and inflammation. Cytokine Growth Factor Rev. 1999, 10: 5-14. source
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- Interpretationreasoning
Loss of IGF-1 is associated with a cachectic situation due to the growth-promoting activity of IGF-1 in muscle.
“Loss of IGF-1 will be associated with a cachectic situation due to the growth-promoting activity of this hormone in muscle.”
Quote in the paperSubstantial claim - Interpretationcitation
Cortisol and noradrenaline support each other in release of energy-rich fuels or calcium/phosphorus from stores.
“Since cortisol and noradrenaline are often cooperative in their individual functions by increasing the respective signaling pathway of the β-adrenoceptor and glucocorticoid receptor type α (for example, [55,56]), these two hormones support each other in release of energy-rich fuels or calcium/phosphorus from stores.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [55] Gruol DJ, Campbell NF, Bourgeois S: Cyclic AMP-dependent protein kinase promotes glucocorticoid receptor function. J Biol Chem. 1986, 261: 4909-4914. source
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- Interpretationreasoning
Thyroid hormones are major energy expenditure hormones.
“Thus, thyroid hormones are major energy expenditure hormones.”
Quote in the paperSubstantial claim0 of 5 sources checked- cites [63] Fox CS, Pencina MJ, D’Agostino RB, Murabito JM, Seely EW, Pearce EN, Vasan RS: Relations of thyroid function to body weight: cross-sectional and longitudinal observations in a community-based sample. Arch Intern Med. 2008, 168: 587-592. source
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- Premisecitation
In chronic inflammatory diseases such as rheumatoid arthritis and systemic lupus erythematosus, hyperinsulinemia and insulin resistance have been described.
“In CIDs such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), hyperinsulinemia and insulin resistance were described [85-87].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [85] Svenson KL, Lundqvist G, Wide L, Hallgren R: Impaired glucose handling in active rheumatoid arthritis: relationship to the secretion of insulin and counter-regulatory hormones. Metabolism. 1987, 36: 940-943. source
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- Interpretationreasoning
A program with long-term elevation of cortisol is not positively selected because of the danger of immunosuppression and sepsis.
“However, a program with long-term elevation of cortisol is not positively selected, because of the danger of immunosuppression and sepsis.”
Quote in the paperSubstantial claim - Interpretationcitation
Androgens are anabolic hormones leading to storage of energy-rich substrates and calcium and phosphorus.
“This short summary clearly identifies androgens as anabolic hormones leading to storage of energy-rich substrates and calcium and phosphorus.”
Quote in the paperNot a substantial claim0 of 4 sources checked- cites [19] Kenyon AT, Knowlton K, Sandiford I: The anabolic effect of the androgens and somatic growth in man. Ann Intern Med. 1944, 20: 632-654. source
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- Interpretationreasoning
All functions of the sympathetic nervous system are related to allocation of energy-rich fuels and calcium and phosphate to an activated immune system.
“All these functions of the SNS are related to allocation of energy-rich fuels and calcium and phosphate to an activated immune system.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [48] Brodows RG, Pi S, Campbell RG: Sympathetic control of hepatic glycogenolysis during glucopenia in man. Metabolism. 1975, 24: 617-624. source
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- Premisecitation
IGF-1 levels are typically decreased in chronic inflammation.
“IGF-1 levels are typically decreased in chronic inflammation [88-90].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [88] Bennett AE, Silverman ED, Miller JJ, Hintz RL: Insulin-like growth factors I and II in children with systemic onset juvenile arthritis. J Rheumatol. 1988, 15: 655-658.
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- Premisecitation
IGF-1 resistance has been described in patients with rheumatoid arthritis.
“In addition, IGF-1 resistance was described in patients with RA [60]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [60] Sarzi-Puttini P, Atzeni F, Scholmerich J, Cutolo M, Straub RH: Anti-TNF antibody therapy improves glucocorticoid- induced insulin-like growth factor-1 (IGF-1) resistance without influencing myoglobin and IGF-1 binding proteins 1 and 3. Ann Rheum Dis. 2005, 65: 301-305. source
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- Interpretationcitation
The role of estrogens is bi-modal in that both storage and release of energy-rich fuels have been described.
“In conclusion, the role of estrogens is bi-modal in that both storage and release of energy-rich fuels have been described.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Barros RP, Gustafsson JA: Estrogen receptors and the metabolic network. Cell Metab. 2011, 14: 289-299. source
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- Interpretationreasoning
Angiotensin II, a major hormone of the RAAS, supports re-allocation of energy-rich fuels and calcium/phosphorus to an activated immune system.
“Thus, similar to the SNS with its major neurotransmitters noradrenaline/adrenaline, angiotensin II, a major hormone of the RAAS, supports re-allocation of energy-rich fuels and calcium/phosphorus to an activated immune system.”
Quote in the paperSubstantial claim0 of 4 sources checked- cites [73] Strazzullo P, Galletti F: Impact of the renin-angiotensin system on lipid and carbohydrate metabolism. Curr Opin Nephrol Hypertens. 2004, 13: 325-332. source
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- Interpretationreasoning
There are two major networks, one that stores energy-rich fuels and one that releases energy-rich fuels upon stressful life events such as acute inflammation, psychological stress, trauma/hemorrhage, pain, and mental illness.
“It turns out that there are two major networks, one that stores energy-rich fuels and one that releases energy-rich fuels upon stressful life events such as acute inflammation (systemic infectious disease or injury), psychological stress, trauma/hemorrhage, pain, and mental illness.”
Quote in the paperSubstantial claim - Interpretationreasoning
In the fasting and in the feeding situation, the vagus nerve is responsible for energy storage.
“Thus, in the fasting and in the feeding situation, the vagus nerve is responsible for energy storage.”
Quote in the paperSubstantial claim0 of 5 sources checked- cites [38] Szekely M: The vagus nerve in thermoregulation and energy metabolism. Auton Neurosci. 2000, 85: 26-38. source
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- Premisecitation
Androgens are mainly anti-inflammatory.
“Whereas androgens are mainly anti-inflammatory [92,93], estrogens have a bi-modal pro- and anti-inflammatory role.”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Sympathetic neurotransmitters can have anti-inflammatory effects on monocytes, macrophages, natural killer cells, neutrophils, and T helper type 1 lymphocytes via β2-adrenergic receptors.
“Since sympathetic neurotransmitters can have anti-inflammatory effects on monocytes, macrophages, natural killer cells, neutrophils, and T helper type 1 lymphocytes via β2-adrenergic receptors, increased activity of the SNS might be favorable in local inflammation [116].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [116] Pongratz G, Straub RH: Role of peripheral nerve fibres in acute and chronic inflammation in arthritis. Nat Rev Rheumatol. 2013, 9: 117-126. source
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- Premisecitation
Local density of sympathetic nerve fibers is markedly reduced in inflamed tissue of different chronic inflammatory diseases and in secondary lymphoid organs of animals with chronic inflammatory diseases, which is a pro-inflammatory signal.
“However, it was observed that local density of sympathetic nerve fibers is markedly reduced in inflamed tissue of different CIDs and in secondary lymphoid organs of animals with CIDs, which is a pro-inflammatory signal recently summarized [116].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [116] Pongratz G, Straub RH: Role of peripheral nerve fibres in acute and chronic inflammation in arthritis. Nat Rev Rheumatol. 2013, 9: 117-126. source
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- Premisecitation
Estrogens have a bi-modal pro- and anti-inflammatory role.
“estrogens have a bi-modal pro- and anti-inflammatory role.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [27] Straub RH: The complex role of estrogens in inflammation. Endocr Rev. 2007, 28: 521-574. source
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- Premisecitation
Vitamin D is an important factor in the development of tolerogenic dendritic cells and T regulatory lymphocytes.
“Vitamin D is an important factor in the development of tolerogenic dendritic cells and T regulatory lymphocytes [101].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [101] Nikolic T, Roep BO: Regulatory multitasking of tolerogenic dendritic cells - lessons taken from vitamin D3-treated tolerogenic dendritic cells. Front Immunol. 2013, 4: 113- source
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- Interpretationreasoning
Loss of IGF-1 and IGF-1 resistance diminish the stores of energy-rich fuels and auxiliary factors in muscles, fat tissue, and bone, thereby serving the activated immune system.
“Thus, loss of IGF-1 and IGF-1 resistance will diminish the stores for energy-rich fuels and auxiliary factors in muscles, fat tissue, and bone, thereby serving the activated immune system (Figure 3).”
Quote in the paperSubstantial claim - Premisecitation
Hypovitaminosis D is a general phenomenon in many chronic inflammatory diseases.
“Hypovitaminosis D is a general phenomenon in many CIDs [100].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [100] Cutolo M, Plebani M, Shoenfeld Y, Adorini L, Tincani A: Vitamin D endocrine system and the immune response in rheumatic diseases. Vitam Horm. 2011, 86: 327-351. source
Not checked in the free run.
- Interpretationreasoning
Loss of androgens together with loss of and resistance to IGF-1 is a critical factor for cachexia and bone loss, leading to loss of energy storage sites in skeletal muscle and bone.
“Loss of androgens together with a loss of and resistance to IGF-1 is a very critical factor for cachexia and bone loss, leading to a loss of energy storage sites in skeletal muscle and bone.”
Quote in the paperSubstantial claim - Premisecitation
Growth hormone given to healthy volunteers slightly but significantly increased serum TNF and serum IL-6.
“Growth hormone given to healthy volunteers slightly but significantly increased serum TNF and serum IL-6 [118].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [118] Andreassen M, Frystyk J, Faber J, Kristensen LO: GH activity and markers of inflammation: a crossover study in healthy volunteers treated with GH and a GH receptor antagonist. Eur J Endocrinol. 2012, 166: 811-819. source
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- Premisecitation
In untreated chronic inflammatory diseases, serum levels of cortisol are usually normal or somewhat higher.
“Similarly, in untreated CIDs, serum levels of cortisol are usually normal or somewhat higher [113], but they are inadequately low to suppress the ongoing inflammatory process.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [113] Jessop DS, Harbuz MS: A defect in cortisol production in rheumatoid arthritis: why are we still looking?. Rheumatology (Oxford). 2005, 44: 1097-1100. source
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- Premisecitation
In chronic inflammatory diseases, estrogen levels remain relatively normal as a consequence of increased conversion of androgens into estrogens in inflamed tissue.
“In CIDs of different etiology, serum androgens are very low [94-96], but estrogen levels remain relatively normal as a consequence of increased conversion of androgens into estrogens in inflamed tissue [97].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [97] Cutolo M, Capellino S, Straub RH: Oestrogens in rheumatic diseases: friend or foe?. Rheumatology (Oxford). 2008, 47: iii2-iii5. source
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- Interpretationreasoning
An anti-inflammatory and energy-storing function of the vagus nerve is probably not available in chronic inflammatory diseases.
“Thus, an anti-inflammatory and energy-storing function of the vagus nerve is probably not available.”
Quote in the paperSubstantial claim - Premisecitation
Treatment with drugs that stimulate growth hormone secretion or treatment with growth hormone can have positive effects in restoring aspects of the aged immune system.
“Treatment with drugs that stimulate growth hormone secretion or treatment with growth hormone can have positive effects in restoring aspects of the aged immune system [117].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [117] Redelman D, Welniak LA, Taub D, Murphy WJ: Neuroendocrine hormones such as growth hormone and prolactin are integral members of the immunological cytokine network. Cell Immunol. 2008, 252: 111-121. source
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- Interpretationreasoning
The consequence of reduced insulin/IGF-1 signaling is a deviation of energy-rich fuels from storage sites (liver, adipose tissue, and muscle) to the activated immune system and inflammatory tissue.
“The consequence is a deviation of energy-rich fuels from storage sites (liver, adipose tissue, and muscle) to the activated immune system and inflammatory tissue.”
Quote in the paperSubstantial claim - Premisecitation
Cortisol is an anti-inflammatory hormone on most occasions.
“Cortisol is an anti-inflammatory hormone on most occasions [111].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [111] Buttgereit F, Burmester GR, Straub RH, Seibel MJ, Zhou H: Exogenous and endogenous glucocorticoids in rheumatic diseases. Arthritis Rheum. 2011, 63: 1-9. source
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- Interpretationreasoning
With respect to osteocalcin, no clear picture emerges as to the help of this hormone in the energy regulation of chronic inflammatory diseases.
“Thus, with respect to osteocalcin, no clear picture emerges as to the help of this hormone in the energy regulation of CIDs.”
Quote in the paperNot a substantial claim - Premisecitation
There is a dissociation between high activity of the sympathetic nervous system and relatively normal activity of the HPA axis in chronic inflammatory diseases.
“There seems to be a dissociation between high activity of the SNS and relatively normal activity of the HPA axis in CIDs [114,115].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [114] Straub RH, Herfarth H, Falk W, Andus T, Schölmerich J: Uncoupling of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis in inflammatory bowel disease?. J Neuroimmunol. 2002, 126: 116-125. source
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- cites [115] Härle P, Straub RH, Wiest R, Mayer A, Schölmerich J, Atzeni F, Carrabba M, Cutolo M, Sarzi-Puttini P: Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamic-pituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems. Ann Rheum Dis. 2006, 65: 51-56. source
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- Premisecitation
The vagus nerve has important anti-inflammatory activities in acute inflammation due to inhibition of TNF.
“The vagus nerve was reported to have important anti-inflammatory activities in acute inflammation due to inhibition of TNF [107].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [107] Tracey KJ: Physiology and immunology of the cholinergic antiinflammatory pathway. J Clin Invest. 2007, 117: 289-296. source
Not checked in the free run.
- Interpretationreasoning
In untreated chronic inflammatory diseases, cortisol levels are inadequately low to suppress the ongoing inflammatory process.
“but they are inadequately low to suppress the ongoing inflammatory process.”
Quote in the paperSubstantial claim - Interpretationreasoning
Local fat accumulation would serve regional storage of energy-rich fuels.
“Such a local accumulation would serve regional storage of energy-rich fuels.”
Quote in the paperSubstantial claim - Premisecitation
In patients with chronic inflammatory diseases, serum levels of osteocalcin have been described as decreased, increased, or normal.
“In regard to serum levels of osteocalcin, decreased, increased, or normal levels have been described in patients with CIDs [102-106].”
Quote in the paperNot a substantial claim0 of 5 sources checked- cites [102] Sambrook PN, Ansell BM, Foster S, Gumpel JM, Hesp R, Reeve J, Zanelli JM: Bone turnover in early rheumatoid arthritis. 1. Biochemical and kinetic indexes. Ann Rheum Dis. 1985, 44: 575-579. source
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- cites [103] Als OS, Riis BJ, Gotfredsen A, Christiansen C, Deftos LJ: Biochemical markers of bone turnover in rheumatoid arthritis. Relation to anti-inflammatory treatment, sex, and menopause. Acta Med Scand. 1986, 219: 209-213. source
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- cites [104] Magaro M, Altomonte L, Mirone L, Zoli A, Corvino G: Bone GLA protein (BGP) levels and bone turnover in rheumatoid arthritis. Br J Rheumatol. 1989, 28: 207-211. source
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- cites [105] Gevers G, Devos P, De RM, Dequeker J: Increased levels of osteocalcin (serum bone Gla-protein) in rheumatoid arthritis. Br J Rheumatol. 1986, 25: 260-262. source
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- cites [106] Pietschmann P, Machold KP, Wolosczuk W, Smolen JS: Serum osteocalcin concentrations in patients with rheumatoid arthritis. Ann Rheum Dis. 1989, 48: 654-657. source
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- Interpretationreasoning
The sympathetic nervous system can have a disease-propagating role in animal models of arthritis.
“This can also be the reason for a disease-propagating role of the SNS in animal models of arthritis (summarized in [116]).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [116] Pongratz G, Straub RH: Role of peripheral nerve fibres in acute and chronic inflammation in arthritis. Nat Rev Rheumatol. 2013, 9: 117-126. source
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- Premisecitation
There is a long-standing activation of the sympathetic nervous system in chronic inflammatory diseases.
“In contrast to transient cortisol increase, there exists a long-standing activation of the SNS in CIDs [110].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [110] Dekkers JC, Geenen R, Godaert GL, Bijlsma JW, van Doornen LJ: Elevated sympathetic nervous system activity in patients with recently diagnosed rheumatoid arthritis with active disease. Clin Exp Rheumatol. 2004, 22: 63-70.
Not checked in the free run.
- Premisecitation
In chronic inflammatory diseases of different etiology, serum androgens are very low.
“In CIDs of different etiology, serum androgens are very low [94-96], but estrogen levels remain relatively normal as a consequence of increased conversion of androgens into estrogens in inflamed tissue [97].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [94] Masi AT, Josipovic DB, Jefferson WE: Low adrenal androgenic-anabolic steroids in women with rheumatoid arthritis (RA): gas–liquid chromatographic studies of RA patients and matched normal control women indicating decreased 11-deoxy-17-ketosteroid excretion. Semin Arthritis Rheum. 1984, 14: 1-23. source
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- cites [95] Cutolo M, Balleari E, Giusti M, Monachesi M, Accardo S: Sex hormone status of male patients with rheumatoid arthritis: evidence of low serum concentrations of testosterone at baseline and after human chorionic gonadotropin stimulation. Arthritis Rheum. 1988, 31: 1314-1317. source
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- cites [96] Straub RH, Vogl D, Gross V, Lang B, Schölmerich J, Andus T: Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease. Am J Gastroenterol. 1998, 93: 2197-2202. source
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- Premisecitation
Differential regulation of local thyroid hormone availability depends mainly on expression of activating (D1 or D2) and inactivating (D3) deiodinases.
“The differential regulation of local thyroid hormone availability depends mainly on expression of activating (D1 or D2) and inactivating (D3) deiodinases [136].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [136] Boelen A, Kwakkel J, Fliers E: Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev. 2011, 32: 670-693. source
Not checked in the free run.
- Interpretationreasoning
In patients with chronic inflammatory diseases, growth hormone serum levels behave similarly to cortisol serum levels, with no clear increase or decrease.
“Thus, in patients with CIDs, growth hormone serum levels behave similarly to cortisol serum levels. In other words, there is no clear increase or decrease of hormone levels in serum.”
Quote in the paperSubstantial claim - Interpretationreasoning
Usual concentrations of hormones of the hypothalamic-pituitary-thyroid gland axis exert many stimulatory effects on the immune system and inflammation.
“Although thyroid hormones have also some anti-inflammatory actions, usual concentrations of hormones of the hypothalamic-pituitary-thyroid gland axis exert many stimulatory effects on the immune system and inflammation.”
Quote in the paperSubstantial claim - Interpretationreasoning
Long-standing use of neuroendocrine pathways is in itself a disease-aggravating etiologic factor in chronic inflammatory diseases.
“Thus, long-standing use of neuroendocrine pathways is in itself a disease-aggravating etiologic factor.”
Quote in the paperSubstantial claim- Rests on an assumption: In epidemiological studies, insulin resistance, cachexia, osteoporosis, and volume overload/hypertension are related to higher mortality and morbidity in chronic inflammatory diseases.
- Premisecitation
ACE inhibitors of different types reduce severity of collagen type II-induced arthritis.
“ACE inhibitors of different types reduce severity of collagen type II-induced arthritis [139,140].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [139] Dalbeth N, Edwards J, Fairchild S, Callan M, Hall FC: The non-thiol angiotensin-converting enzyme inhibitor quinapril suppresses inflammatory arthritis. Rheumatology (Oxford). 2005, 44: 24-31. source
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- cites [140] Sagawa K, Nagatani K, Komagata Y, Yamamoto K: Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice. Arthritis Rheum. 2005, 52: 1920-1928. source
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- Premisecitation
It seems likely that levels of thyroid hormones are low in chronic rheumatic diseases as demonstrated in systemic lupus erythematosus and Kawasaki disease.
“Although not many studies in chronic rheumatic diseases exist, it seems likely that levels of thyroid hormones are low as demonstrated in SLE and Kawasaki disease [133,134].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [133] Kumar K, Kole AK, Karmakar PS, Ghosh A: The spectrum of thyroid disorders in systemic lupus erythematosus. Rheumatol Int. 2012, 32: 73-78. source
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- cites [134] Hashimoto H, Igarashi N, Yachie A, Miyawaki T, Hashimoto T, Sato T: The relationship between serum levels of interleukin-6 and thyroid hormone during the follow-up study in children with nonthyroidal illness: marked inverse correlation in Kawasaki and infectious disease. Endocr J. 1996, 43: 31-38. source
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- Premisecitation
Thyroid hormones are required for normal B-cell production in the bone marrow.
“Thyroid hormones are required for normal B-cell production in the bone marrow [130].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [130] Foster MP, Montecino-Rodriguez E, Dorshkind K: Proliferation of bone marrow pro-B cells is dependent on stimulation by the pituitary/thyroid axis. J Immunol. 1999, 163: 5883-5890. source
Not checked in the free run.
- Interpretationreasoning
The long-term use of neuroendocrine pathways used in acute inflammatory illness is harmful.
“However, the long-term use of these pathways is harmful.”
Quote in the paperSubstantial claim - Premisecitation
The anti-inflammatory role of endogenous cortisol in chronic inflammatory diseases was visualized by blocking endogenous cortisol production with metyrapone.
“However, the anti-inflammatory role of endogenous cortisol was visualized in CIDs by blocking endogenous cortisol production with metyrapone [122].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [122] Saldanha C, Tougas G, Grace E: Evidence for anti-inflammatory effect of normal circulating plasma cortisol. Clin Exp Rheumatol. 1986, 4: 365-366.
Not checked in the free run.
- Premisecitation
Angiotensin II via AT1 receptors is a pro-inflammatory factor in a lupus mouse model.
“Angiotensin II via AT1 receptors is also a pro-inflammatory factor in a lupus mouse model [138].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [138] Crowley SD, Vasievich MP, Ruiz P, Gould SK, Parsons KK, Pazmino AK, Facemire C, Chen BJ, Kim HS, Tran TT, Pisetsky DS, Barisoni L, Prieto-Carrasquero MC, Jeansson M, Foster MH, Coffman TM: Glomerular type 1 angiotensin receptors augment kidney injury and inflammation in murine autoimmune nephritis. J Clin Invest. 2009, 119: 943-953.
Not checked in the free run.
- Premisecitation
Patients with sepsis demonstrate increased activity of the RAAS.
“Patients with sepsis demonstrate increased activity of the RAAS [143].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [143] Doerschug KC, Delsing AS, Schmidt GA, Ashare A: Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis. Crit Care. 2010, 14: R24- source
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- Premisecitation
Acute infectious disease leads to upregulation of the RAAS system in a mouse model of cytomegalovirus infection.
“Acute infectious disease leads to upregulation of the RAAS system in a mouse model of cytomegalovirus infection [141].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [141] Cheng J, Ke Q, Jin Z, Wang H, Kocher O, Morgan JP, Zhang J, Crumpacker CS: Cytomegalovirus infection causes an increase of arterial blood pressure. PLoS Pathog. 2009, 5: e1000427- source
Not checked in the free run.
- Premisecitation
In different organs such as kidney, heart, and vasculature, angiotensin II induces an inflammatory response by fostering expression of pro-inflammatory chemokines responsible for tissue accumulation of immunocompetent cells.
“In different organs such as kidney, heart, and vasculature, angiotensin II induces an inflammatory response by fostering the expression of pro-inflammatory chemokines, responsible for tissue accumulation of immunocompetent cells [137].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [137] Benigni A, Cassis P, Remuzzi G: Angiotensin II revisited: new roles in inflammation, immunology and aging. EMBO Mol Med. 2010, 2: 247-257. source
Not checked in the free run.
- Premisecitation
Thyroid hormones can bind to integrin αvβ3 to switch on a cascade of signaling events through MAPK, phospholipase C, proteinkinase Cα, ERK1/2, and/or hypoxia-inducible factor-1, leading to enhanced cytokine and growth factor action and angiogenesis.
“Thyroid hormones can bind to the integrin αvβ3 to switch on a cascade of signaling events through MAPK, phospholipase C, proteinkinase Cα, ERK1/2, and/or hypoxia-inducible factor-1, leading to enhanced cytokine and growth factor action and angiogenesis [128].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [128] De VP, Incerpi S, Pedersen JZ, Luly P, Davis FB, Davis PJ: Thyroid hormones as modulators of immune activities at the cellular level. Thyroid. 2011, 21: 879-890. source
Not checked in the free run.
- Interpretationreasoning
All mechanisms of non-thyroidal illness syndrome lead to inhibition of the hypothalamic-pituitary-thyroid gland axis.
“All mechanisms lead to inhibition of the hypothalamic-pituitary-thyroid gland axis.”
Quote in the paperSubstantial claim - Interpretationreasoning
Since the RAAS exerts pro-inflammatory effects in addition to its function as an energy expenditure hormonal system, it is able to support the re-allocation of energy-rich fuels to the activated immune system.
“Since the RAAS exerts pro-inflammatory effects in addition to its function as an energy expenditure hormonal system, it is perfectly able to support the re-allocation of energy-rich fuels to the activated immune system.”
Quote in the paperNot a substantial claim - Premisecitation
Injection of lipopolysaccharide into rats increased activity of the RAAS system.
“Injection of lipopolysaccharide into rats increased activity of the RAAS system [142].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [142] Ohtani R, Ohashi Y, Muranaga K, Itoh N, Okamoto H: Changes in activity of the renin-angiotensin system of the rat by induction of acute inflammation. Life Sci. 1989, 44: 237-241. source
Not checked in the free run.
- Interpretationcitation
All of these findings indicate that the RAAS is activated in acute and chronic inflammation.
“In conclusion, all of these findings indicate that the RAAS is activated in acute and chronic inflammation.”
Quote in the paperSubstantial claim - Interpretationreasoning
In chronic and acute inflammation, there seems to exist a rapid downregulation of the hypothalamic-pituitary-thyroid gland axis.
“In summary, in chronic and acute inflammation, there seems to exist a rapid downregulation of the hypothalamic-pituitary-thyroid gland axis.”
Quote in the paperSubstantial claim - Premisecitation
Local RAAS pathways support pro-inflammatory, proliferative, and profibrotic activities via angiotensin type 1 receptors that couple to Gq and Gαi.
“While systemic effects of angiotensin II are related to hemodynamic and metabolic functions (see above), local RAAS pathways support pro-inflammatory, proliferative, and profibrotic activities via angiotensin type (AT)1 receptors that couple to G proteins of the type Gq and Gαi (recently summarized in [137]).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [137] Benigni A, Cassis P, Remuzzi G: Angiotensin II revisited: new roles in inflammation, immunology and aging. EMBO Mol Med. 2010, 2: 247-257. source
Not checked in the free run.
- Premisecitation
Downregulation of the central part of the hypothalamic-pituitary-thyroid gland axis during acute and chronic inflammation does not necessarily induce decreased thyroid hormone levels in key metabolic organs such as liver, muscle, and adipose tissue.
“Importantly, recent experimental studies have shown that downregulation of the central part of this axis observed during acute and chronic inflammation does not necessarily induce decreased thyroid hormone levels in key metabolic organs such as liver, muscle, and adipose tissue (summarized in [136]).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [136] Boelen A, Kwakkel J, Fliers E: Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev. 2011, 32: 670-693. source
Not checked in the free run.
- Premisecitation
A recent investigation in patients with rheumatoid arthritis found a decrease in TSH levels during TNF-neutralizing therapy.
“A recent investigation in patients with RA found a decrease in TSH levels during TNF-neutralizing therapy [135].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [135] Raterman HG, Jamnitski A, Lems WF, Voskuyl AE, Dijkmans BA, Bos WH, Simsek S, Lips P, van de Stadt RJ, de Koning MH, Nurmohamed MT: Improvement of thyroid function in hypothyroid patients with rheumatoid arthritis after 6 months of adalimumab treatment: a pilot study. J Rheumatol. 2011, 38: 247-251. source
Not checked in the free run.
- Premisecitation
Growth hormone serum levels were lower, normal, or slightly elevated in patients with rheumatoid arthritis and systemic lupus erythematosus.
“Growth hormone serum levels were lower, normal, or slightly elevated in patients with RA and SLE (summarized in [121]).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [121] Denko CW, Malemud CJ: Role of the growth hormone/insulin-like growth factor-1 paracrine axis in rheumatic diseases. Semin Arthritis Rheum. 2005, 35: 24-34. source
Not checked in the free run.
- May combine two claims. 42
- Classified as probably not a substantial claim. 3
May combine two claims.
FindingcitationChronic smoldering inflammation in humans is established with elevations of serum IL-6 from normal levels of 1 pg/mL to approximately 10 to 100 pg/mL, leading to an increase of resting metabolic rate in healthy volunteers.
“Chronic smoldering inflammation in humans is already established with elevations of serum IL-6 from normal levels of 1 pg/mL to approximately 10 to 100 pg/mL of serum IL-6, leading to an increase of resting metabolic rate in healthy volunteers [8].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [8] Tsigos C, Papanicolaou DA, Defensor R, Mitsiadis CS, Kyrou I, Chrousos GP: Dose effects of recombinant human interleukin-6 on pituitary hormone secretion and energy expenditure. Neuroendocrinology. 1997, 66: 54-62. source
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Findingnone givenIn chronic inflammatory diseases, a preponderance of energy expenditure pathways is switched on, leading to typical hormonal changes such as insulin/IGF-1 resistance, hypoandrogenemia, hypovitaminosis D, mild hypercortisolemia, and increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system.
“In chronic inflammatory diseases, a preponderance of energy expenditure pathways is switched on, leading to typical hormonal changes such as insulin/IGF-1 resistance, hypoandrogenemia, hypovitaminosis D, mild hypercortisolemia, and increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationInflammation-driven energy expenditure programs were positively selected for acute but not chronic systemic inflammation, and chronic use of these programs is highly unfavorable.
“(iii) evolutionary medicine explains that these inflammation-driven energy expenditure programs were positively selected for acute but not chronic systemic inflammation, and chronic use of these programs is highly unfavorable [7].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [7] Straub RH, Besedovsky HO: Integrated evolutionary, immunological, and neuroendocrine framework for the pathogenesis of chronic disabling inflammatory diseases. FASEB J. 2003, 17: 2176-2183. source
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InterpretationreasoningIGF-1 is an important storage hormone for energy-rich fuels and for factors auxiliary to the immune system such as calcium and phosphorus.
“Thus, IGF-1 is an important storage hormone for energy-rich fuels and for factors auxiliary to the immune system such as calcium and phosphorus.”
Quote in the paperNot a substantial claim0 of 4 sources checked- cites [15] Stitt TN, Drujan D, Clarke BA, Panaro F, Timofeyva Y, Kline WO, Gonzalez M, Yancopoulos GD, Glass DJ: The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. Mol Cell. 2004, 14: 395-403. source
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- cites [16] Michal G: Biochemical Pathways. 1999, Heidelberg Berlin: Spektrum Akademischer Verlag
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- cites [17] Blüher S, Kratzsch J, Kiess W: Insulin-like growth factor I, growth hormone and insulin in white adipose tissue. Best Pract Res Clin Endocrinol Metab. 2005, 19: 577-587. source
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- cites [18] Kawai M, Rosen CJ: The insulin-like growth factor system in bone: basic and clinical implications. Endocrinol Metab Clin North Am. 2012, 41: 323-333. source
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May combine two claims.
PremisecitationLeukocytes cannot become insulin-resistant but upregulate GLUT1, GLUT3, and GLUT4 transporters upon activation.
“This is relevant for leukocytes that, importantly, cannot become insulin-resistant but upregulate GLUT1, GLUT3, and GLUT4 transporters upon activation [14].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [14] Calder PC, Dimitriadis G, Newsholme P: Glucose metabolism in lymphoid and inflammatory cells and tissues. Curr Opin Clin Nutr Metab Care. 2007, 10: 531-540. source
Not checked in the free run.
May combine two claims.
Premisenone givenAging, chronic psychological stress, and mental illnesses are accompanied by chronic smoldering inflammation.
“Since aging, chronic psychological stress, and mental illnesses are also accompanied by chronic smoldering inflammation (such as in CID), many aspects apply to age- and stress-related diseases and mental illness.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationcitationOsteocalcin supports insulin function and thus storage of energy-rich fuels in adipose tissue and muscle.
“Nevertheless, these studies indicate that osteocalcin supports insulin function and thus storage of energy-rich fuels in adipose tissue and muscle.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [31] Neve A, Corrado A, Cantatore FP: Osteocalcin: skeletal and extra-skeletal effects. J Cell Physiol. 2013, 228: 1149-1153. source
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- cites [32] Lee NK, Karsenty G: Reciprocal regulation of bone and energy metabolism. Trends Endocrinol Metab. 2008, 19: 161-166. source
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- cites [33] Hwang YC, Jeong IK, Ahn KJ, Chung HY: The uncarboxylated form of osteocalcin is associated with improved glucose tolerance and enhanced beta-cell function in middle-aged male subjects. Diabetes Metab Res Rev. 2009, 25: 768-772. source
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InterpretationreasoningCortisol via many independent pathways belongs to the network of energy-expenditure hormones, an increase of which leads to rapid allocation of energy-rich fuels to the immune system.
“In conclusion, cortisol via many independent pathways belongs to the network of energy-expenditure hormones, an increase of which leads to rapid allocation of energy-rich fuels to the immune system.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [43] Darmaun D, Matthews DE, Bier DM: Physiological hypercortisolemia increases proteolysis, glutamine, and alanine production. Am J Physiol. 1988, 255: E366-E373.
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- cites [44] Djurhuus CB, Gravholt CH, Nielsen S, Mengel A, Christiansen JS, Schmitz OE, Moller N: Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans. Am J Physiol Endocrinol Metab. 2002, 283: E172-E177. source
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- cites [45] Gathercole LL, Morgan SA, Bujalska IJ, Hauton D, Stewart PM, Tomlinson JW: Regulation of lipogenesis by glucocorticoids and insulin in human adipose tissue. PLoS One. 2011, 6: e26223- source
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PremisecitationAcute inflammatory situations such as systemic infectious diseases induce an energy re-allocation program with three major pathways: release of energy-rich fuels from storage sites into circulation; inhibition of uptake of energy-rich fuels into liver, muscle, and fat tissue by intentionally induced insulin resistance; and inhibition of growth-related and reproductive functions.
“This can happen in acute inflammatory situations such as systemic infectious diseases, which induce an energy re-allocation program with three major pathways: (i) release of energy-rich fuels from storage sites into circulation (liver glucose, muscle amino acids, glycerol, and free fatty acids from fat tissue), (ii) inhibition of uptake of energy-rich fuels into liver, muscle, and fat tissue by”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [4] Straub RH, Cutolo M, Buttgereit F, Pongratz G: Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J Intern Med. 2010, 267: 543-560. source
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PremisecitationThe renin-angiotensin-aldosterone system induces insulin resistance on local and systemic levels, which explains why therapies that interfere with the RAAS reduce the incidence of type 2 diabetes mellitus.
“Apart from its major function of sodium and water retention, the RAAS was found to induce insulin resistance on local and systemic levels, which explains why therapies that interfere with the RAAS reduce the incidence of type 2 diabetes mellitus [71-73].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [71] Luther JM, Brown NJ: The renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011, 32: 734-739. source
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- cites [72] Lastra-Lastra G, Sowers JR, Restrepo-Erazo K, Manrique-Acevedo C, Lastra-Gonzalez G: Role of aldosterone and angiotensin II in insulin resistance: an update. Clin Endocrinol (Oxf). 2009, 71: 1-6. source
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- cites [73] Strazzullo P, Galletti F: Impact of the renin-angiotensin system on lipid and carbohydrate metabolism. Curr Opin Nephrol Hypertens. 2004, 13: 325-332. source
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May combine two claims.
InterpretationreasoningBoth the insulin and IGF-1 receptor pathways are not intact in chronic inflammatory diseases.
“Thus, both pathways through insulin and IGF-1 receptors are not intact in CIDs.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningVitamin D is responsible for storage of calcium/phosphorus in bone and amino acids in muscle.
“In summary, vitamin D is responsible for storage of calcium/phosphorus in bone and amino acids in muscle.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [28] Nicolaysen R: Studies upon the mode of action of vitamin D: the influence of vitamin D on the absorption of calcium and phosphorus in the rat. Biochem J. 1937, 31: 122-129. source
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- cites [29] Haussler MR, Whitfield GK, Kaneko I, Haussler CA, Hsieh D, Hsieh JC, Jurutka PW: Molecular mechanisms of vitamin D action. Calcif Tissue Int. 2013, 92: 77-98. source
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- cites [30] Girgis CM, Clifton-Bligh RJ, Hamrick MW, Holick MF, Gunton JE: The roles of vitamin D in skeletal muscle: form, function, and metabolism. Endocr Rev. 2013, 34: 33-83. source
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Probably not a substantial claim: may not pass S4 (based).
InterpretationreasoningThe chronic misuse of the energy expenditure system leads to the known systemic disease sequelae in chronic inflammatory diseases.
“The chronic misuse of the energy expenditure system leads to the known systemic disease sequelae in chronic inflammatory diseases (see below).”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationcitationInsulin resistance is the critical determinant of the pro- or anti-inflammatory effect of insulin, because only liver, muscle, and fat tissue, but not leukocytes, become insulin-resistant.
“It is proposed that insulin resistance is the critical determinant of the pro- or anti-inflammatory effect of insulin, because only liver, muscle, and fat tissue, but not leukocytes, become insulin-resistant [14].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [14] Calder PC, Dimitriadis G, Newsholme P: Glucose metabolism in lymphoid and inflammatory cells and tissues. Curr Opin Clin Nutr Metab Care. 2007, 10: 531-540. source
Not checked in the free run.
May combine two claims.
InterpretationreasoningIn chronic inflammatory diseases, insulin-mediated uptake of energy-rich fuels into liver, muscle, and fat is diminished, while direct activation of local immune cells by insulin remains possible.
“For insulin, uptake of energy-rich fuels into liver, muscle, and fat will be diminished, but direct activation of local immune cells will still be possible (Figure 3).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationGrowth hormone accelerates recovery of the immune system following transplantation of various cell types, and it replenished the severely affected T-cell compartment in patients with HIV.
“Growth hormone accelerates recovery of the immune system following transplantation of various cell types, and it replenished the severely affected T-cell compartment in patients with HIV [117].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [117] Redelman D, Welniak LA, Taub D, Murphy WJ: Neuroendocrine hormones such as growth hormone and prolactin are integral members of the immunological cytokine network. Cell Immunol. 2008, 252: 111-121. source
Not checked in the free run.
May combine two claims.
InterpretationreasoningBoth vagal hypoactivity and sympathetic hyperactivity would support ongoing inflammation in chronic inflammatory diseases.
“Both aspects would support ongoing inflammation in CIDs.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
InterpretationreasoningSlightly elevated cortisol might support bone breakdown to deliver auxiliary factors such as calcium and phosphorus to activated immune cells.
“Slightly elevated cortisol might also support bone breakdown in order to deliver auxiliary factors such as calcium and phosphorus to activated immune cells.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationGrowth hormone was made responsible for the chronic smoldering inflammation during aging, which can be studied in growth hormone pathway-deficient mice that demonstrate less inflammation and increased longevity.
“Growth hormone was made responsible for the chronic smoldering inflammation during aging, which can be studied in growth hormone pathway-deficient mice that demonstrate less inflammation and increased longevity [119].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [119] Masternak MM, Bartke A: Growth hormone, inflammation and aging. Pathobiol Aging Age Relat Dis. 2012, 2: 17293- source
Not checked in the free run.
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PremisecitationImmune cells carry the growth hormone receptor, and growth hormone signaling involves JAK2-STAT-Ras-MAPK pathways that are shared by cytokine signaling pathways.
“Immune cells carry the growth hormone receptor, and growth hormone signaling involves JAK2-STAT-Ras-MAPK pathways that are shared by cytokine signaling pathways (summarized in [117]).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [117] Redelman D, Welniak LA, Taub D, Murphy WJ: Neuroendocrine hormones such as growth hormone and prolactin are integral members of the immunological cytokine network. Cell Immunol. 2008, 252: 111-121. source
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PremisecitationPro-inflammatory factors such as TNF reduce signaling of insulin and IGF-1 and production of IGF-1 from liver.
“Pro-inflammatory factors such as tumor necrosis factor (TNF) reduce signaling of insulin and IGF-1 and production of IGF-1 from liver (for example, [91]).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [91] Hotamisligil GS: Inflammatory pathways and insulin action. Int J Obes Relat Metab Disord. 2003, 27: S53-S55. source
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May combine two claims.
PremisecitationGrowth hormone primes neutrophils for production of lysosomal enzymes and superoxide anions, supports survival of memory T cells, increases immunoglobulin secretion of B cells, and stimulates thymulin secretion by thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst, and killing capacity of neutrophils or macrophages.
“Furthermore, growth hormone primes neutrophils for production of lysosomal enzymes and superoxide anions, supports survival of memory T cells, increases immunoglobulin secretion of B cells, and stimulates thymulin secretion by thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst, and killing capacity of neutrophils or macrophages [120].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [120] Kelley KW, Weigent DA, Kooijman R: Protein hormones and immunity. Brain Behav Immun. 2007, 21: 384-392. source
Not checked in the free run.
May combine two claims.
InterpretationreasoningThe program of reduced insulin/IGF-1 signaling affects liver, adipose tissue, and muscle, but not immune cells.
“This program affects liver, adipose tissue, and muscle, but not immune cells, because they cannot become insulin-resistant.”
Quote in the paperSubstantial claim- Rests on an assumption: Immune cells cannot become insulin-resistant.
May combine two claims.
PremisecitationVitamin D fosters many aspects of innate immunity but inhibits adaptive immunity toward a T helper type 1 and T helper type 17 direction.
“Vitamin D was described to foster many aspects of innate immunity but inhibits adaptive immunity toward a T helper type 1 and T helper type 17 direction [100].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [100] Cutolo M, Plebani M, Shoenfeld Y, Adorini L, Tincani A: Vitamin D endocrine system and the immune response in rheumatic diseases. Vitam Horm. 2011, 86: 327-351. source
Not checked in the free run.
May combine two claims.
InterpretationreasoningHigher activity of the sympathetic nervous system supports provision of energy-rich fuels on a systemic level but probably has no favorable anti-inflammatory effects in inflamed tissue.
“Thus, a higher activity of the SNS supports provision of energy-rich fuels on a systemic level but probably has no favorable anti-inflammatory effects in inflamed tissue.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningSomewhat elevated cortisol levels would serve insulin resistance and glucose/free fatty acid provision to the activated immune system, but at these levels one does not expect many anti-inflammatory effects.
“Somewhat elevated cortisol levels would serve insulin resistance and glucose/free fatty acid provision to the activated immune system, but at these levels one does not expect many anti-inflammatory effects (inadequate levels in relation to inflammation).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationEstrogens stimulate B cell-dominated immune reactions supported by T helper type 2 responses, whereas they inhibit T helper type 1 and macrophage-dominated immune responses.
“Thus, B cell-dominated immune reactions that are supported by T helper type 2 immune responses are stimulated, whereas T helper type 1 and macrophage-dominated immune responses are inhibited.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [27] Straub RH: The complex role of estrogens in inflammation. Endocr Rev. 2007, 28: 521-574. source
Not checked in the free run.
May combine two claims.
PremisecitationChronic inflammation such as in rheumatoid arthritis is accompanied by vagal hypoactivity and sympathetic hyperactivity.
“However, chronic inflammation such as in RA is accompanied by vagal hypoactivity and sympathetic hyperactivity [108-110].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [108] Sloan RP, McCreath H, Tracey KJ, Sidney S, Liu K, Seeman T: RR interval variability is inversely related to inflammatory markers: the CARDIA study. Mol Med. 2007, 13: 178-184. source
Not checked in the free run.
- cites [109] Bruchfeld A, Goldstein RS, Chavan S, Patel NB, Rosas-Ballina M, Kohn N, Qureshi AR, Tracey KJ: Whole blood cytokine attenuation by cholinergic agonists ex vivo and relationship to vagus nerve activity in rheumatoid arthritis. J Intern Med. 2010, 268: 94-101. source
Not checked in the free run.
- cites [110] Dekkers JC, Geenen R, Godaert GL, Bijlsma JW, van Doornen LJ: Elevated sympathetic nervous system activity in patients with recently diagnosed rheumatoid arthritis with active disease. Clin Exp Rheumatol. 2004, 22: 63-70.
Not checked in the free run.
May combine two claims.
InterpretationreasoningLoss of vitamin D may support the inflammatory process and general osteoporosis, which would serve the immune system by providing calcium and phosphorus.
“Thus, loss of vitamin D may support the inflammatory process but also general osteoporosis, which would serve the immune system by providing calcium and phosphorus.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationTransgenic mice overexpressing growth hormone or its receptor exhibit overgrowth of the thymus and spleen and display increases in mitogenic responses to Concanavalin A.
“Transgenic mice overexpressing growth hormone or its receptor exhibit overgrowth of the thymus and spleen and display increases in mitogenic responses to Concanavalin A [120].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [120] Kelley KW, Weigent DA, Kooijman R: Protein hormones and immunity. Brain Behav Immun. 2007, 21: 384-392. source
Not checked in the free run.
May combine two claims.
PremisecitationIn juvenile forms of chronic inflammatory diseases, growth hormone can have favorable growth-promoting but not anti-inflammatory effects.
“Indeed, in juvenile forms of CIDs, growth hormone can have favorable growth-promoting but not anti-inflammatory effects (summarized in [127]).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [127] Pozzo AM, Kemp SF: Growth and growth hormone treatment in children with chronic diseases. Endocrinol Metab Clin North Am. 2012, 41: 747-759. source
Not checked in the free run.
May combine two claims.
PremisecitationElevation of systemic inflammation such as during injury, inflammation, or starvation leads to the non-thyroidal illness syndrome, which has features including downregulation of hypothalamic thyrotropin-releasing hormone, lowered secretion of TSH, free T4, and free T3, decreased levels of circulating free T3 due to decreased peripheral T4→T3 conversion, and increased metabolism of biologically活跃 T
“Elevation of systemic inflammation such as during injury, inflammation, or starvation leads to the non-thyroidal illness syndrome, which has the following features [131]: (a) downregulation of hypothalamic thyrotropin-releasing hormone; (b) lowered secretion of TSH, free T4, and free T3; (c) decreased levels of circulating free T3 due to decreased peripheral T4→T3 conversion; and (d) increased”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [131] Huang SA, Bianco AC: Reawakened interest in type III iodothyronine deiodinase in critical illness and injury. Nat Clin Pract Endocrinol Metab. 2008, 4: 148-155. source
Not checked in the free run.
May combine two claims.
PremisecitationAfter injection of IL-6 into healthy volunteers, T4 and free T4 increased after 4 hours but T3 levels were reduced 24 hours later, indicating a rapid downregulation of T3 by IL-6.
“After injection of IL-6 into healthy volunteers, T4 and free T4 increased after 4 hours but T3 levels were reduced 24 hours later, which indicates a rapid downregulation of this biologically active hormone by IL-6 [132].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [132] Torpy DJ, Tsigos C, Lotsikas AJ, Defensor R, Chrousos GP, Papanicolaou DA: Acute and delayed effects of a single-dose injection of interleukin-6 on thyroid function in healthy humans. Metabolism. 1998, 47: 1289-1293. source
Not checked in the free run.
May combine two claims.
PremisecitationTwo Russian studies identified increased levels of angiotensin II and aldosterone in patients with rheumatoid arthritis and systemic lupus erythematosus, but this awaits further confirmation.
“Two Russian studies identified increased levels of angiotensin II and aldosterone in patients with RA and SLE, but this awaits further confirmation [145,146].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [145] Samoriadova OS, Zharova EA, Masenko VP, Balabanova RM, Vil’chinskaia MI, Nasonov EL: The renin-angiotensin-aldosterone system and arterial hypertension in patients with rheumatoid arthritis. Klin Med (Mosk). 1991, 69: 69-71.
Not checked in the free run.
- cites [146] Shilkina NP, Stoliarova SA, Iunonin IE, Driazhenkova IV: Neurohumoral regulation of blood pressure in rheumatic patients. Ter Arkh. 2009, 81: 37-41.
Not checked in the free run.
May combine two claims.
InterpretationreasoningMany neuroendocrine pathways support immune activation, which in light of autoimmunity or immunity toward harmless microbes in the gut/skin/respiratory tract is a misused program.
“It turns out that many neuroendocrine pathways support immune activation (third column in Table 2), which in light of autoimmunity or immunity toward harmless microbes in the gut/skin/respiratory tract is a misused program.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
InterpretationreasoningThe stimulating effects of thyroid hormones on phagocytosis and killing might be explained by release of inorganic iodide independent of genomic effects via thyroid hormone receptors.
“This is a very attractive concept because it might well explain the stimulating effects of thyroid hormones on phagocytosis and killing independent of genomic effects via thyroid hormone receptors.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningIn addition to inducing immune activation, many reported neuroendocrine mechanisms induce insulin resistance, cachexia, osteoporosis, and volume overload/hypertension.
“In addition to inducing immune activation, many reported neuroendocrine mechanisms induce insulin resistance, cachexia, osteoporosis, and volume overload/hypertension (water retention).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationDuring acute inflammation, in muscle, the hormone-activating deiodinase D2 increases whereas the hormone-inactivating D3 decreases, leading to higher muscular T3 levels and increased breakdown of energy-rich substrates in muscle only.
“For example, during acute inflammation, in the muscle, the hormone-activating deiodinase D2 increases whereas the hormone-inactivating D3 decreases, which would lead to higher muscular T3 levels, resulting in increased breakdown of energy-rich substrates in the muscle only [136].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [136] Boelen A, Kwakkel J, Fliers E: Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev. 2011, 32: 670-693. source
Not checked in the free run.
May combine two claims.
PremisecitationThyroid hormones induce oxygen radical production in neutrophils, IFN-γ-stimulated major histocompatibility complex class II expression, IL-6, IL-8, and IL-12 secretion from different cell types, lymphocyte proliferation, IFN-γ-stimulated natural killer cell activity, and superoxide anion production in human alveolar neutrophils and macrophages.
“Thyroid hormones induce oxygen radical production in neutrophils [128], IFN-γ-stimulated major histocompatibility complex class II expression [128], IL-6, IL-8, and IL-12 secretion from different cell types [128], lymphocyte proliferation [128], IFN-γ-stimulated natural killer cell activity [128], and superoxide anion production in human alveolar neutrophils and macrophages [129].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [128] De VP, Incerpi S, Pedersen JZ, Luly P, Davis FB, Davis PJ: Thyroid hormones as modulators of immune activities at the cellular level. Thyroid. 2011, 21: 879-890. source
Not checked in the free run.
- cites [129] Nishizawa Y, Fushiki S, Amakata Y: Thyroxine-induced production of superoxide anion by human alveolar neutrophils and macrophages: a possible mechanism for the exacerbation of bronchial asthma with the development of hyperthyroidism. In Vivo. 1998, 12: 253-257.
Not checked in the free run.
May combine two claims.
InterpretationreasoningWater retention with RAAS hormones is of outstanding importance, possibly leading to volume overload.
“In addition, water retention with these hormones will be of outstanding importance, possibly leading to volume overload.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationIn granulocytes, the inactivating D3 is highly expressed, and release of inorganic iodide is related to improved killing of bacteria.
“In granulocytes, the inactivating D3 is highly expressed [136]. In these cells, the release of inorganic iodide was related to improved killing of bacteria [136].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [136] Boelen A, Kwakkel J, Fliers E: Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev. 2011, 32: 670-693. source
Not checked in the free run.
May combine two claims.
PremisecitationSomatostatin has direct suppressive effects on immune cells and nociceptive nerve fibers.
“Although somatostatin has direct suppressive effects on immune cells and nociceptive nerve fibers [126], somatostatin might also block growth hormone release on a systemic level in the pituitary gland.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [126] Imhof AK, Gluck L, Gajda M, Lupp A, Brauer R, Schaible HG, Schulz S: Differential antiinflammatory and antinociceptive effects of the somatostatin analogs octreotide and pasireotide in a mouse model of immune-mediated arthritis. Arthritis Rheum. 2011, 63: 2352-2362. source
Not checked in the free run.
May combine two claims.
PremisecitationIn chronic inflammation, D2 and D3 are elevated and the net effect on T3 is a reduction in active T3.
“This is different in chronic inflammation, where D2 and D3 are elevated and, as was described, the net effect on T3 is a reduction in active T3 [136].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [136] Boelen A, Kwakkel J, Fliers E: Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev. 2011, 32: 670-693. source
Not checked in the free run.
May combine two claims.
PremisecitationACE is upregulated in synovial tissue of patients with rheumatoid arthritis, leading to higher availability of angiotensin II in inflamed joints.
“ACE is upregulated in synovial tissue of patients with RA, leading to higher availability of angiotensin II in inflamed joints [144].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [144] Walsh DA, Catravas J, Wharton J: Angiotensin converting enzyme in human synovium: increased stromal [(125)I]351A binding in rheumatoid arthritis. Ann Rheum Dis. 2000, 59: 125-131. source
Not checked in the free run.
May combine two claims.
PremisecitationOpen therapies with the growth hormone inhibitor somatostatin in small studies demonstrated anti-inflammatory effects such as reduction of synovial membrane thickness and improved clinical symptoms such as morning stiffness and other American College of Rheumatology criteria in rheumatoid arthritis.
“Open therapies with the growth hormone inhibitor somatostatin in small studies demonstrated anti-inflammatory effects such as reduction of synovial membrane thickness [123] and improved clinical symptoms such as morning stiffness and other American College of Rheumatology criteria in RA [124,125].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [123] Coari G, Di FM, Iagnocco A, Di Novi MR, Mauceri MT, Ciocci A: Intra-articular somatostatin 14 reduces synovial thickness in rheumatoid arthritis: an ultrasonographic study. Int J Clin Pharmacol Res. 1995, 15: 27-32.
Not checked in the free run.
- cites [124] Paran D, Elkayam O, Mayo A, Paran H, Amit M, Yaron M, Caspi D: A pilot study of a long acting somatostatin analogue for the treatment of refractory rheumatoid arthritis. Ann Rheum Dis. 2001, 60: 888-891. source
Not checked in the free run.
- cites [125] Koseoglu F, Koseoglu T: Long acting somatostatin analogue for the treatment of refractory RA. Ann Rheum Dis. 2002, 61: 573-574. source
Not checked in the free run.
The paper relies on this without support.
Immune cells cannot become insulin-resistant.
“This program affects liver, adipose tissue, and muscle, but not immune cells, because they cannot become insulin-resistant.”
The paper relies on this without support.
In epidemiological studies, insulin resistance, cachexia, osteoporosis, and volume overload/hypertension are related to higher mortality and morbidity in chronic inflammatory diseases.
“In epidemiological studies, these elements were related to higher mortality and morbidity in CIDs.”
The paper relies on this without support.
Elevated sympathetic nervous tone stimulates sodium and water retention and bone loss, which support the activated immune system.
“In addition, an elevated sympathetic nervous tone stimulates sodium and water retention and bone loss, which support the activated immune system.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In a prospective cohort, anti-inflammatory therapies with anti-integrin vedolizumab and anti-TNF agents infliximab or adalimumab resulted in improved sleep quality within 6 weeks of therapy initiation.
“In a prospective cohort, anti-inflammatory therapies with anti-integrin (vedolizumab) and anti-TNF agents (infliximab or adalimumab) resulted in improved sleep quality (assessed with PROMIS) within 6 wk of therapy initiation (527).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [527]
Comparable effects of anti-TNF therapy on sleep were found in patients with IBD and ankylosing spondylitis.
“Comparable effects of anti-TNF therapy on sleep were found in patients with IBD and ankylosing spondylitis (282, 527).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [527]
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The Dark Side of Testosterone Deficiency: II. Type 2 Diabetes and Insulin Resistance
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“In the fasting situation, vagal afferents are important in transferring hepatoportal information on low blood glucose and low levels of other nutrients to the dorsal vagal complex, leading to hunger signals, inhibition of sympathetic activation, inhibition of efferent vagal activation, hypometabolism, and hypothermia…”
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BackgroundINCREASED LEVELS OF OSTEOCALCIN (SERUM BONE GLA-PROTEIN) IN RHEUMATOID ARTHRITIS
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“ACE is upregulated in synovial tissue of patients with RA, leading to higher availability of angiotensin II in inflamed joints [144].”
BackgroundAssociation between obesity, metabolic risks and serum osteocalcin level in postmenopausal women
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“of insulin resistance’ [34].”
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“Open therapies with the growth hormone inhibitor somatostatin in small studies demonstrated anti-inflammatory effects such as reduction of synovial membrane thickness [123] and improved clinical symptoms such as morning stiffness and other American College of Rheumatology criteria in RA [124,125].”
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“Under natural conditions in the wild, the situation is balanced in that storage and expenditure are similar (for example, [11]).”
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“Although somatostatin has direct suppressive effects on immune cells and nociceptive nerve fibers [126], somatostatin might also block growth hormone release on a systemic level in the pituitary gland.”
BackgroundTHE ANABOLIC EFFECTS OF THE ANDROGENS AND SOMATIC GROWTH IN MAN
KENYON, A. T., KNOWLTON, K., & SANDIFORD, I. (1944) · Annals of Internal Medicine · doi:10.7326/0003-4819-20-4-632 · Cited by 50 · see citing works
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Energy metabolism and rheumatic diseases: from cell to organism
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“org/licenses/ medium, provided the original work is proper 2014 (i) energy-rich fuel allocation is important for an activated immune system [4,5], (ii) increased activity of the water retention system accompanies energy allocation to the immune system [6], and (iii) evolutionary medicine explains that these inflammati…”
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“In addition, IGF-1 resistance was described in patients with RA [60], and IGF-1 levels are typically decreased in chronic inflammation [88-90].”
BackgroundSympathetic control of hepatic glycogenolysis during glucopenia in man
Brodows, R. G., Pi-Sunyer, F. X., & Campbell, R. G. (1975) · Metabolism · doi:10.1016/0026-0495(75)90141-9 · Cited by 45 · cited 1× · see citing works
“The SNS innervates the liver and supports hepatic glycogenolysis and gluconeogenesis, leading to release of glucose [48].”
BackgroundRATERMAN, H. G., JAMNITSKI, A., LEMS, W. F., VOSKUYL, A. E., DIJKMANS, B. A. C., BOS, W. H., SIMSEK, S., LIPS, P., van de STADT, R. J., de KONING, M. H. M. T., et al. (2011) · The Journal of Rheumatology · doi:10.3899/jrheum.100488 · Cited by 45 · cited 1× · see citing works
“A recent investigation in patients with RA found a decrease in TSH levels during TNF-neutralizing therapy [135].”
BackgroundMechanisms Behind the Anti-inflammatory Actions of Insulin
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“In recent years, insulin was categorized as an antiinflammatory hormone because it is able to remove energy-rich fuels such as glucose and free fatty acids from circulation that would nourish the immune system [81,82].”
BackgroundBone turnover in early rheumatoid arthritis. 1. Biochemical and kinetic indexes.
Sambrook, P. N., Ansell, B. M., Foster, S., Gumpel, J. M., Hesp, R., Reeve, J., & Zanelli, J. M. (1985) · Annals of the Rheumatic Diseases · doi:10.1136/ard.44.9.575 · Cited by 43 · see citing works
Insulin-like growth factors I and II in children with systemic onset juvenile arthritis.
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“Growth hormone via IGF-1 increases net whole-body protein synthesis and, thus, growth hormone has some anabolic effects [57], which might change during inflammatory illness because of growth hormone receptor resistance and loss of pulsatile growth hormone secretion [58-61].”
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“However, insulin is also directly responsible for growth-related processes [13].”
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Impact of growth hormone hypersecretion on the adult human kidney
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“natriuretic effects, thereby adding to water and sodium retention [62].”
BackgroundSerum osteocalcin concentrations in patients with rheumatoid arthritis.
Pietschmann, P., Machold, K. P., Wolosczuk, W., & Smolen, J. S. (1989) · Annals of the Rheumatic Diseases · doi:10.1136/ard.48.8.654 · Cited by 28 · cited 1× · see citing works
“In regard to serum levels of osteocalcin, decreased, increased, or normal levels have been described in patients with CIDs [102-106].”
BackgroundDimitriadis, G., Maratou, E., Alevizaki, M., Boutati, E., Psara, K., Papasteriades, C., & Raptis, S. A. (2005) · Hormone and Metabolic Research · doi:10.1055/s-2005-861026 · Cited by 28 · cited 1× · see citing works
“GLUT4 glucose transporters in the skeletal muscle and monocytes [64-66].”
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Changes in activity of the renin-angiotensin system of the rat by induction of acute inflammation
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“creased activity of the RAAS system [142].”
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Treat obesity as physiology, not physics
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“mainly by circulating glucose [12].”
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“Although not many studies in chronic rheumatic diseases exist, it seems likely that levels of thyroid hormones are low as demonstrated in SLE and Kawasaki disease [133,134].”
BackgroundBONE GLA PROTEIN (BGP) LEVELS AND BONE TURNOVER IN RHEUMATOID ARTHRITIS
MAGARO, M., ALTOMONTE, L., MIRONE, L., ZOLI, A., & CORVINO, G. (1989) · Rheumatology · doi:10.1093/rheumatology/28.3.207 · Cited by 18 · cited 1× · see citing works
“In regard to serum levels of osteocalcin, decreased, increased, or normal levels have been described in patients with CIDs [102-106].”
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Hypothalamic regulation of muscle metabolism
Braun, T. P., & Marks, D. L. (2011) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e328345bbcd · Cited by 17 · cited 1× · see citing works
“It was suggested that the SNS is a regulator of muscle catabolism [51].”
BackgroundLong acting somatostatin analogue for the treatment of refractory RA
Koseoglu, F., Koseoglu, T., Paran, D., Elkayam, O., Paran, H., Yaron, M., & Caspi, D. (2002) · Annals of the Rheumatic Diseases · doi:10.1136/ard.61.6.573 · Cited by 17 · cited 1× · see citing works
“Open therapies with the growth hormone inhibitor somatostatin in small studies demonstrated anti-inflammatory effects such as reduction of synovial membrane thickness [123] and improved clinical symptoms such as morning stiffness and other American College of Rheumatology criteria in RA [124,125].”
BackgroundAn Old Friend in a New Light: The Role of Osteocalcin in Energy Metabolism
Sullivan, T. R., Duque, G., KEECH, A. C., & Herrmann, M. (2011) · Cardiovascular Therapeutics · doi:10.1111/j.1755-5922.2011.00300.x · Cited by 16 · cited 1× · see citing works
“Several other reports link high osteocalcin levels to insulin sensitivity [31], but studies in humans have not yet shown direct causal effects [35].”
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“Finally, one of the major hormones to release energyrich fuels from storage sites, namely glucocorticoid, reduces osteocalcin levels in that it inhibits osteoblast function [37].”
BackgroundInsulin, glucocorticoids and the control of inflammatory responses.
Garcia-Leme, J., Zb, F., Sannomiya, P., et al. (1992) · PubMed · Cited by 16 · see citing works
Growth and Growth Hormone Treatment in Children with Chronic Diseases
Pozzo, A. M., & Kemp, S. F. (2012) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2012.07.001 · Cited by 9 · cited 2× · see citing works
“Growth hormone might be judged in a different way in juvenile forms of CIDs because of anabolic effects on muscle and bone growth [127].”
Background[Neurohumoral regulation of blood pressure in rheumatic patients].
Np, S., Столярова, С. А., Юнонин, И. Е., et al. (2009) · PubMed · Cited by 5 · see citing works
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Hepatic Growth Hormone Resistance After Acute Injury
Corrick, R. M., Li, L., Frank, S. J., et al. (2013) · Endocrinology · doi:10.1210/en.2012-2134 · Cited by 4 · cited 1× · see citing works
“Growth hormone via IGF-1 increases net whole-body protein synthesis and, thus, growth hormone has some anabolic effects [57], which might change during inflammatory illness because of growth hormone receptor resistance and loss of pulsatile growth hormone secretion [58-61].”
Background
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- Michal G: Biochemical Pathways. 1999, Heidelberg Berlin: Spektrum Akademischer Verlag
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The Sleep-Immune Crosstalk in Health and Disease
Besedovsky, L., Lange, T., & Haack, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00010.2018 · Cited by 1,479 · see citing works
Effects of stress on immune function: The good, the bad, and the beautiful
Dhabhar, F. S. (2014) · Immunologic Research · doi:10.1007/s12026-014-8517-0 · Cited by 1,343 · see citing works
The physical frailty syndrome as a transition from homeostatic symphony to cacophony
Fried, L. P., Cohen, A. A., Xue, Q., Walston, J. D., Bandeen‐Roche, K., & Varadhan, R. (2021) · Nature Aging · doi:10.1038/s43587-020-00017-z · Cited by 591 · see citing works
Dhabhar, F. S. (2018) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2018.03.004 · Cited by 333 · see citing works
Straub, R. H., & Carsten Schradin, A. (2016) · Evolution Medicine and Public Health · doi:10.1093/emph/eow001 · Cited by 234 · see citing works
“concepts from the field of bodily energy regulation were added (13-15).”
BackgroundSelf-citationInflammation, physical activity, and chronic disease: An evolutionary perspective
Burini, R. C., Anderson, E., Durstine, J. L., & Carson, J. A. (2020) · Sports Medicine and Health Science · doi:10.1016/j.smhs.2020.03.004 · Cited by 166 · see citing works
Glucocorticoids and chronic inflammation
Straub, R. H., & Cutolo, M. (2016) · Lara D. Veeken · doi:10.1093/rheumatology/kew348 · Cited by 149 · see citing works
Self-citationWhite, C. M., Pasupuleti, V., Roman, Y. M., Li, Y., & Hernández, A. V. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.104280 · Cited by 115 · see citing works
Lewczuk, B., Redlarski, G., Żak, A. J., Ziółkowska, N., Przybylska‐Gornowicz, B., & Krawczuk, M. (2014) · BioMed Research International · doi:10.1155/2014/169459 · Cited by 103 · see citing works
“Cortisol governs hunger and appetite, stress, inflammatory response, and many other functions [108–110].”
BackgroundSickness behaviors across vertebrate taxa: proximate and ultimate mechanisms
Lopes, P. C., French, S. S., Woodhams, D. C., & Binning, S. A. (2021) · Journal of Experimental Biology · doi:10.1242/jeb.225847 · Cited by 96 · see citing works
“Inhibition of the somatotropic and hypothalamic–pituitary–thyroid axes (see Glossary) has also been found under immune challenges (Kondo et al., 1997; Soto et al., 1998; Straub, 2014).”
BackgroundKemenade, B. M. L. V.-V., Cohen, N., & Chadzińska, M. (2016) · Developmental & Comparative Immunology · doi:10.1016/j.dci.2016.05.015 · Cited by 96 · see citing works
“In contrast, reduced levels of estrogens (e.g., during menopause), are correlated with increased secretion by T cells and macrophages/dendritic cells of TNF-a, IFN-g and TGF-b secretion (Straub, 2014).”
BackgroundEndometriosis and polycystic ovary syndrome are diametric disorders
Dinsdale, N. L., & Crespi, B. J. (2021) · Evolutionary Applications · doi:10.1111/eva.13244 · Cited by 90 · see citing works
“Reduced testosterone, or hypoandrogenemia, is characteristic of chronic inflammatory diseases— a diverse range of conditions that involve long- term immune activation— as testosterone generally promotes energy storage and thus inhibits metabolically costly inflammation (Straub, 2014).”
BackgroundPathogenicity and virulence of Bordetella pertussis and its adaptation to its strictly human host
Belcher, T., Dubois, V., Rivera-Millot, A., Locht, C., & Jacob‐Dubuisson, F. (2021) · Virulence · doi:10.1080/21505594.2021.1980987 · Cited by 83 · see citing works
Frew, J. W., Hawkes, J. E., & Krueger, J. G. (2019) · Therapeutic Advances in Chronic Disease · doi:10.1177/2040622319830646 · Cited by 82 · see citing works
IGF-1 and IGFBP-3 in Inflammatory Cachexia
Martı́n, A. I., Priego, T., Moreno‐Rupérez, Á., González‐Hedström, D., Granado, M., & López‐Calderón, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22179469 · Cited by 75 · see citing works
“This neuroendocrine response is an adaptive or stress response, which leads to the release of energy substrates from their storage in adipose tissue, liver, and skeletal muscle, in order to be consumed by the activated immune system [1].”
BackgroundBruner‐Tran, K. L., Ding, T., Yeoman, K. B., Archibong, A. E., Arosh, J. A., & Osteen, K. G. (2014) · PLoS ONE · doi:10.1371/journal.pone.0105084 · Cited by 73 · see citing works
“Since testicular inflammation has also previously been associated with impaired steroidogenesis in men [43], we next examined serum levels of testosterone in our animals.”
BackgroundEnvironmental Endocrine Disruptors and Endometriosis
Rumph, J. T., Stephens, V. R., Archibong, A. E., Osteen, K. G., & Bruner‐Tran, K. L. (2020) · Advances in anatomy, embryology and cell biology · doi:10.1007/978-3-030-51856-1_4 · Cited by 74 · see citing works
“Equally important is the fact that hormones influence inflammatory response (Straub 2014); thus, alterations in response to these steroids would likely have far-reaching effects in multiple systems.”
BackgroundAbatacept Improves Whole-Body Insulin Sensitivity in Rheumatoid Arthritis
Ursini, F., Russo, E., Hribal, M. L., Mauro, D., Savarino, F., Bruno, C., Tripolino, C., Rubino, M., Naty, S., & Grembiale, R. D. (2015) · Medicine · doi:10.1097/md.0000000000000888 · Cited by 69 · see citing works
“A strict connection between inflammation and IR has been uncovered in the last years.(19,20) Tumor necrosis factor-alpha (TNF-a), a proinflammatory cytokine involved in the pathophysiology of RA, has been demonstrated to be involved in this link.”
BackgroundEffect of curcumin on proinflammatory cytokines: A meta-analysis of randomized controlled trials
Gorabi, A. M., Razi, B., Aslani, S., Abbasifard, M., Imani, D., Sathyapalan, T., & Sahebkar, A. (2021) · Cytokine · doi:10.1016/j.cyto.2021.155541 · Cited by 69 · see citing works
“Additionally, chronic inflammation increases the risk of various malignancies [1-5].”
BackgroundPathogen manipulation of host metabolism: A common strategy for immune evasion
Freyberg, Z., & Harvill, E. T. (2017) · PLoS Pathogens · doi:10.1371/journal.ppat.1006669 · Cited by 63 · see citing works
van der Spoel, E., Roelfsema, F., & van Heemst, D. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.619568 · Cited by 62 · see citing works
“TSH is highly responsive to different stressors, including inflammation (90) and environmental endocrine disrupters (89).”
BackgroundThyroid hormone and the stunned myocardium
Novitzky, D., & Cooper, D. K. C. (2014) · Journal of Endocrinology · doi:10.1530/joe-14-0389 · Cited by 58 · see citing works
“T3/T4 play an important role in intracellular homeostasis of ionized calcium (Straub 2014), thereby avoiding calcium-induced injury (Oshiro et al.”
BackgroundThe Role of Calcium in Inflammation-Associated Bone Resorption
Klein, G. L. (2018) · Biomolecules · doi:10.3390/biom8030069 · Cited by 52 · see citing works
“This concept is not new and is briefly mentioned by Straub [6] in his review of the pathophysiology of chronic inflammatory disease.”
BackgroundInfluentialComprehending the Role of Endocrine Disruptors in Inducing Epigenetic Toxicity
Kirtana, A., & Seetharaman, B. (2022) · Endocrine Metabolic & Immune Disorders - Drug Targets · doi:10.2174/1871530322666220411082656 · Cited by 53 · see citing works
Ortega, M. A., Fraile‐Μartinez, O., Montero, C. G., Haro, S., Álvarez-Mon, M. Á., León-Oliva, D. D., Gomez-Lahoz, A. M., Monserrat, J., Atienza-Pérez, M., Díaz, D., et al. (2023) · Military Medical Research · doi:10.1186/s40779-023-00461-z · Cited by 53 · see citing works
Gorabi, A. M., Abbasifard, M., Imani, D., Aslani, S., Razi, B., Alizadeh, S., Bagheri‐Hosseinabadi, Z., Sathyapalan, T., & Sahebkar, A. (2021) · Phytotherapy Research · doi:10.1002/ptr.7284 · Cited by 50 · see citing works
Mohammadi, H., Talebi, S., Ghavami, A., Rafiei, M., Sharifi, S., Faghihimani, Z., Ranjbar, G., Miraghajani, M. S., & Askari, G. (2021) · Journal of Trace Elements in Medicine and Biology · doi:10.1016/j.jtemb.2021.126857 · Cited by 49 · see citing works
Reich, W., Bilkenroth, U., Schubert, J., et al. (2015) · Journal of Cranio-Maxillofacial Surgery · doi:10.1016/j.jcms.2015.07.035 · Cited by 48 · see citing works
de Araújo, G. G., Papoti, M., dos Reis, I. G. M., de Mello, M. A. R., & Gobatto, C. A. (2016) · Frontiers in Physiology · doi:10.3389/fphys.2016.00505 · Cited by 47 · see citing works
“Furthermore, the reduction in white blood cell and cortiscosterone may be related with energy-rich fuel allocation, glycogen synthesis (Straub, 2014).”
BackgroundMechanical transduction by ion channels: A cautionary tale
Sachs, F. (2015) · World Journal of Neurology · doi:10.5316/wjn.v5.i3.74 · Cited by 47 · see citing works
Zhai, J., Li, Z., Zhou, Y., & Yang, X. (2022) · Journal of Reproductive Immunology · doi:10.1016/j.jri.2022.103490 · Cited by 43 · see citing works
Association Between Keratoconus and Thyroid Gland Dysfunction: A Cross-Sectional Case–Control Study
Elmassry, A., Doheim, M. F., Iqbal, M., et al. (2020) · Journal of Refractive Surgery · doi:10.3928/1081597x-20200226-03 · Cited by 41 · see citing works
Low Progesterone and Low Estradiol Levels Associate With Abdominal Aortic Aneurysms in Men
Ohlsson, C., Langenskiöld, M., Smidfelt, K., POUTANEN, M. H., Ryberg, H., Norlén, A., Nordanstig, J., Bergström, G. M. L., & Tivesten, Å. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab867 · Cited by 41 · see citing works
Calton, E. K., Keane, K. N., Soares, M. J., Rowlands, J., & Newsholme, P. (2016) · Redox Biology · doi:10.1016/j.redox.2016.10.007 · Cited by 41 · see citing works
“Such observations mimic the increased energetic cost of an activated immune system [51].”
BackgroundGaspari, L., Paris, F., Kalfa, N., Soyer‐Gobillard, M., Sultan, C., & Hamamah, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22169091 · Cited by 37 · see citing works
“reported a non-significant reduction in the serum level of testosterone [61,62], a wellknown consequence of chronic inflammation in men [85].”
BackgroundThe effect of chronic inflammation on female fertility
Ameho, S., & Klutstein, M. (2025) · Reproduction · doi:10.1530/rep-24-0197 · Cited by 39 · see citing works
“In diseases with a component of chronic in fl ammation of different etiology, serum androgens are very low (Straub et al. 1998, Straub 2014), but estrogen levels remain relatively normal as a consequence of increased conversion of androgens into estrogens in the in fl amed tissue (Cutolo et al. 2008).”
The emerging role of bile acids in white adipose tissue
Schmid, A., Karrasch, T., & Schäffler, A. (2023) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2023.08.002 · Cited by 33 · see citing works
Immune-Mediated Diseases from the Point of View of Psychoneuroimmunoendocrinology
Ortega, M. A., Montero, C. G., Fraile‐Μartinez, O., Álvarez-Mon, M. Á., Gomez-Lahoz, A. M., Lahera, G., Monserrat, J., Rodríguez–Jiménez, R., Quintero, J., & Álvarez‐Mon, M. (2022) · Biology · doi:10.3390/biology11070973 · Cited by 33 · see citing works
“RAAS promotes insulin resistance and the release of norepinephrine by the SNS, which directs great energy resources to the cells of the IS [41].”
BackgroundPruimboom, L., & Muskiet, F. A. J. (2018) · Medical Hypotheses · doi:10.1016/j.mehy.2018.08.002 · Cited by 30 · see citing works
Clinical considerations in the management of hidradenitis suppurativa in women
Kozera, E. K., Lowes, M. A., Hsiao, J. L., et al. (2021) · International Journal of Women’s Dermatology · doi:10.1016/j.ijwd.2021.10.012 · Cited by 29 · see citing works
“Research in other fields has established that sex hormones have immune-modulating (both immune-activating and immune-suppressive) activity on dendritic cells, T-cell maturation, differentiation, and suppression of the Th1 immune response ( Straub, 2014 ).”
BackgroundInfluentialThe causes of drug-induced muscle toxicity
Jones, J. D. G., Kirsch, H. L., Wortmann, R. L., & Pillinger, M. H. (2014) · Current Opinion in Rheumatology · doi:10.1097/bor.0000000000000108 · Cited by 27 · see citing works
Fraile‐Μartinez, O., Álvarez-Mon, M. Á., Montero, C. G., Pekarek, L., Guijarro, L. G., Lahera, G., Sáez, M. A., Monserrat, J., Motogo, D., Quintero, J., et al. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.956923 · Cited by 29 · see citing works
“Likewise, sustained inflammation, gut dysbiosis, and chronic stress may lead to a wide variety of systemic endocrine changes, including insulin resistance, sex hormone dysregulation, or an aberrant functioning of the renin– angiotensin–aldosterone system (RAAS) (65).”
BackgroundOlvera, A., Martyniuk, C. J., Buisine, N., Jacinto, V. J., Sánchez‐Flores, A., Sachs, L. M., & Orozco, A. (2017) · Scientific Reports · doi:10.1038/s41598-017-14913-9 · Cited by 24 · see citing works
Ota, K., Yamagishi, S., Kim, M. S., Dambaeva, S. V., Gilman‐Sachs, A., Beaman, K. D., & Kwak-Kim, J. Y.-H. (2014) · Fertility and Sterility · doi:10.1016/j.fertnstert.2014.06.010 · Cited by 24 · see citing works
Sabbaghziarani, F., Mortezaee, K., Akbari, M., Kashani, I. R., Soleimani, M., Moini, A., Nejad, N. A., Zendedel, A., & Hassanzadeh, G. (2016) · Metabolic Brain Disease · doi:10.1007/s11011-016-9897-8 · Cited by 24 · see citing works
Xu, T., Wu, X., Lu, X., Liang, Y., Mao, Y., Loor, J. J., & Yang, Z. (2021) · BMC Veterinary Research · doi:10.1186/s12917-021-02797-x · Cited by 24 · see citing works
Xu, T., Seyfert, H. M., & Shen, X. (2017) · Journal of Dairy Science · doi:10.3168/jds.2017-12878 · Cited by 22 · see citing works
Thyroid hormone: relevance to xenotransplantation
Iwase, H., Ekser, B., Hara, H., et al. (2016) · Xenotransplantation · doi:10.1111/xen.12243 · Cited by 22 · see citing works
“” Thyroid hormones play an important role in mitochondrial function (generation of high-energy phosphates and prevention of tissue lactic acidosis) and intracellular homeostasis of calcium [8,9].”
BackgroundEriksson, E. S., Rodriguez, M. L., Halvorsen, B. L., Johansson, I., Mårtensson, A. K. F., Wilhelmson, A. S., Huse, C., Ueland, T., Aukrust, P., Broch, K., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-56217-x · Cited by 21 · see citing works
Evolutionary Aspects of Infections: Inflammation and Sickness Behaviors
Dantzer, R. (2022) · Current topics in behavioral neurosciences · doi:10.1007/7854_2022_363 · Cited by 21 · see citing works
Differential modulation of innate immune response by epinephrine and estradiol
Margaryan, S., Hyusyan, A., Martirosyan, A., Sargsian, S., & Manukyan, G. P. (2017) · Hormone Molecular Biology and Clinical Investigation · doi:10.1515/hmbci-2016-0046 · Cited by 20 · see citing works
“Disturbances within these systems may have adverse effect on a variety of immunological mechanisms and lead to immune activation or suppression, depending on the systems being affected and the nature of the stimuli [1], [2].”
BackgroundGorabi, A. M., Aslani, S., Imani, D., Razi, B., Sathyapalan, T., & Sahebkar, A. (2021) · Phytotherapy Research · doi:10.1002/ptr.7262 · Cited by 21 · see citing works
“…(OA), asthma, chronic obstructive pulmonary disease (COPD), Alzheimer's disease (AD), metabolic syndrome, and various malignancies (Aggarwal, 2004; Bagheri-Hosseinabadi, Imani, Yousefi, & Abbasifard, 2020; P. Hunter, 2012; Martinez & White, 2018; Song, Quach, & Liang, 2020; Straub, 2014).”
Inflammatory and Infectious Disorders in Endocrine Pathology
Uccella, S., Dottermusch, M., Erickson, L. A., Warmbier, J., Montone, K. T., & Saeger, W. (2023) · Endocrine Pathology · doi:10.1007/s12022-023-09771-3 · Cited by 19 · see citing works
“The complex interplay between the endocrine and immune systems causes the insurgence of endocrinopathies following severe inflammatory conditions and, in turn, the propensity to develop inflammation as a complication of endocrine diseases [1].”
InfluentialSabbaghziarani, F., Mortezaee, K., Akbari, M., Kashani, I. R., Soleimani, M., Hassanzadeh, G., & Zendedel, A. (2017) · Cell Biochemistry and Function · doi:10.1002/cbf.3244 · Cited by 19 · see citing works
“In contrast with our study, it has been noted the stimulation of proinflammatory cytokines by regular hormone concentrations of the hypothalamic‐pituitary‐thyroid axis; suppression of this axis and the subsequent reduction of T3 bioactivity is a result of inflammation.(18) To explain, we find that proinflammatory cyto…”
ResultOgliari, G., Smit, R. A. J., van der Spoel, E., Mari, D., Torresani, E., Felicetta, I., Lucchi, T. A., Rossi, P. D., van Heemst, D., de Craen, A. J. M., et al. (2016) · The Journals of Gerontology Series A · doi:10.1093/gerona/glw113 · Cited by 19 · see citing works
“Indeed, low normal TSH, especially in conjunction with low fT3, may be indicative of underlying stresses, like inflammation (37,38).”
BackgroundRosique, C., Lebsir, D., Lestaevel, P., Benatia, S., Guigon, P., Caire-Maurisier, F., Benderitter, M., Bennouna, D., Souidi, M., & Martin, J. (2019) · Journal of Toxicology and Environmental Health · doi:10.1080/15287394.2019.1625474 · Cited by 17 · see citing works
“Our findings are in agreement with TSH regulations on bile acids, lipid metabolism, general metabolic regulations, mitochondrial function, and tricarboxylic acid cycle (Mullur, Liu, and Brent 2014), nervous system mediators (neurotransmitters and catecholamines), and oxidative stress (Straub 2014).”
ResultOrtega, M. A., Fraile‐Μartinez, O., Montero, C. G., Dı́az, R., López-González, L., Monserrat, J., Barrena-Blázquez, S., Álvarez-Mon, M. Á., Lahera, G., & Álvarez‐Mon, M. (2024) · Military Medical Research · doi:10.1186/s40779-024-00577-w · Cited by 17 · see citing works
Sickness behavior is delayed in hypothyroid mice
Silva, V. C., & Giusti‐Paiva, A. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.12.014 · Cited by 15 · see citing works
“of catecholamines in the mechanisms of thermoregulation (Little et al., 2013; Warner et al., 2013; Straub, 2014).”
BackgroundInfluentialBulboacă, A. E., Bolboaca, S. D., Bulboacă, A., & Prodan, C. I. (2016) · Archives of Medical Science · doi:10.5114/aoms.2016.60129 · Cited by 15 · see citing works
“Inflammatory disorders (in chronic inflammatory diseases, a preponderance of energy expenditure pathways are switched on and thyroid hormones become energy expenditure hormones [6]) can influence the serum level of thyroid hormones in the elderly population.”
BackgroundArora, P., Singh, K., Kumari, M., & Trivedi, R. (2022) · Metabolomics · doi:10.1007/s11306-022-01886-8 · Cited by 13 · see citing works
“An activated immune system acts as an independent stimulus for endocrine and neuronal changes along with re-location of substrates for energy production (Straub, 2014).”
BackgroundPratap, U. P., Hima, L., Kannan, T., THYAGARAJAN, C., Priyanka, H. P., Vasantharekha, R., Anand, P., & ThyagaRajan, S. (2020) · Archives of Rheumatology · doi:10.46497/archrheumatol.2020.7481 · Cited by 11 · see citing works
Alshelh, Z., Brusaferri, L., Morrissey, E. J., Torrado-Carvajal, Á., Kim, M., Akeju, O., Grmek, G., Chane, C. A., Murphy, J. P., Schrepf, A., et al. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.05.008 · Cited by 9 · see citing works
Rajaiah, R., Pandey, K., Acharya, A., Ambikan, A. T., Kumar, N., Guda, R. S., Avedissian, S. N., Montaner, L. J., Cohen, S. M., Neogi, U., et al. (2024) · iScience · doi:10.1016/j.isci.2024.110501 · Cited by 9 · see citing works
Premature aging in chronic kidney disease and chronic obstructive pulmonary disease
Kooman, J. P., Shiels, P. G., & Stenvinkel, P. (2015) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0000000000000218 · Cited by 9 · see citing works
Lowin, T., Kok, C., Smutny, S., & Pongratz, G. (2022) · Biomedicines · doi:10.3390/biomedicines10051118 · Cited by 10 · see citing works
Efficacy and safety of Barg-e-Sahajna ( Moringa oleifera Lam.) in primary hypothyroidism
Alam, M. A., Quamri, M. A., & Haider, N. (2021) · Drug Metabolism and Personalized Therapy · doi:10.1515/dmpt-2021-0136 · Cited by 9 · see citing works
Zaegel, N., Brahimaj, R., Battaglia-Hsu, S.-F., Lamiral, Z., & Feigerlová, E. (2024) · Journal of the Endocrine Society · doi:10.1210/jendso/bvae099 · Cited by 6 · see citing works
“Low-grade inflammation has been associated with metabolic abnormalities such as metabolic dysfunction-associated steatotic liver disease (MASLD) [17, 18].”
BackgroundA History of Psycho-Neuro-Endocrine Immune Interactions in Rheumatic Diseases
Straub, R. H., & Cutolo, M. (2024) · NeuroImmunoModulation · doi:10.1159/000540959 · Cited by 11 · see citing works
Self-citationCancer on fire: role of inflammation in prevention and treatment
Pandey, M. K., Suskil, M. V., Chitren, R. J., Al‐Odat, O. S., Jonnalagadda, S. C., & Aggarwal, B. B. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823482-2.00024-8 · Cited by 7 · see citing works
Dessein, P. H., Stanwix, A. E., & Solomon, A. (2022) · The Journal of Rheumatology · doi:10.3899/jrheum.220788 · Cited by 7 · see citing works
Elbialy, Z. I., Atef, E., Al‐Hawary, I. I., Salah, A. S., Abo-Shosha, A. A., Abualreesh, M. H., & Assar, D. H. (2023) · Fish Physiology and Biochemistry · doi:10.1007/s10695-022-01165-2 · Cited by 7 · see citing works
“This neuroendocrine response is an adaptive or stress response that causes the release of energy substrates from storage in adipose tissue, liver, and skeletal muscle for the activated immune system to consume them (Straub 2014).”
BackgroundMultisystem derangements in frailty and sarcopenia: a source for biomarker discovery
Picca, A., Calvani, R., & Marzetti, E. (2022) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0000000000000828 · Cited by 7 · see citing works
Wang, Y., Zhu, H., He, L.-C., et al. (2025) · Translational Stroke Research · doi:10.1007/s12975-025-01332-6 · Cited by 6 · see citing works
“Since inflammation may also induce a wide response in the neuroendocrine system [42, 43], our alternative hypothesis is that the inhibition of IGF/IGFBPs is related to chronic inflammation in CSVD; however, the causal relationship between the two is unknown.”
Serum Osteopontin Is Associated With Organ Failure in Patients With Acute Pancreatitis
Swärd, P., Bertilsson, S., Struglics, A., et al. (2018) · Pancreas · doi:10.1097/mpa.0000000000000991 · Cited by 6 · see citing works
“Osteocalcin is a bone-specific protein considered to reflect bone formation(4) and known to decrease in the critically ill patients,(5) but osteocalcin has also recently emerged to have hormonal activity, because it increases insulin production and improves glucose tolerance.(4,6) Our aimswere to investigate serum ost…”
BackgroundEnergiemetabolismus des Immunsystems
Straub, R. H., Pongratz, G., Buttgereit, F., & Gaber, T. (2023) · Zeitschrift für Rheumatologie · doi:10.1007/s00393-023-01389-4 · Cited by 6 · see citing works
Self-citationThe Impact of Physical Activity on Thyroid Health: Insights From Representative Data in Korea
Lee, J., Baek, H.-S., Jo, K., Kim, M., Lee, J. M., Chang, S. A., & Lim, D. (2024) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgae178 · Cited by 7 · see citing works
Yarahmadi, A., Malek, F., Poorhassan, M., Ghaffari, N., Ebrahimi, B., Bazrafkan, M., Mohammed, N. M., Almahafdha, A., & Hassanzadeh, G. (2022) · Journal of Contemporary Medical Sciences · doi:10.22317/jcms.v8i3.1230 · Cited by 6 · see citing works
Ma, H., Sui, G.-Y., Park, J.-S., Wang, F., Ma, Y., Shin, D.-S., Rustamov, N., Jang, J. S., Chang, S. I., Lee, J., et al. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e39534 · Cited by 4 · see citing works
“Moreover, they possess immunosuppressive, anti-inflammatory, antitoxic, and anti-nausea properties [7].”
BackgroundUnveiling estrogen’s role: a comprehensive review of its impact on skin health and disease
Yi, L., Deng, N., Luo, X., Tan, Y., Huang, Z., Liu, Y., Xing, J., Zeng, Y., & Yi, J. (2026) · APOPTOSIS · doi:10.1007/s10495-025-02244-4 · Cited by 4 · see citing works
“Estrogen operates through immune modulation mechanisms independent of classic estrogen response elements [143 ].”
Rodrigues, B., Mathias, L. S., Depra, I. D. C., Cury, S., de Oliveira, M., Olimpio, R., Sibio, M. D. D., Gonçalves, B. M., & Nogueira, C. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.886136 · Cited by 2 · see citing works
“The THs triiodothyronine (T3) and thyroxine (T4) are especially essential for bone development and maintenance (Bassett et al., 2003; Straub, 2014), as changes in their levels may affect bone metabolism and cause abnormalities, such as changes in the bone mineral density (Waung et al., 2012; Kim…”
BackgroundThe safety of Bruton's tyrosine kinase inhibitors in B‐cell malignancies: A systematic review
Arustamyan, M., Kibrik, P., Hatipoğlu, D., Bungo, B., Mentias, A. G., Hill, B. T., & Moudgil, R. (2022) · European Journal Of Haematology · doi:10.1111/ejh.13854 · Cited by 4 · see citing works
Yan, G., Li, J., Su, Y., Li, G., Feng, G., Liu, J., Gao, X., & Zhou, H. (2025) · Frontiers in Surgery · doi:10.3389/fsurg.2024.1433751 · Cited by 4 · see citing works
Efficacy and safety of Barg-e-Sahajna (Moringa olifera Lam.) in primary hypothyroidism
Alam, M. A., Quamri, M. A., & Haider, N. (2021) · Drug Metabolism and Personalized Therapy · doi:10.1515/dmdi-2021-0136 · Cited by 4 · see citing works
Wang, X., Meng, S., Xiao, X., Liu, L., Chen, H., Li, Y., Zhang, R., Jiang, Q., Liu, S., & Gao, R. (2026) · Journal of Medical Internet Research · doi:10.2196/84617 · Cited by 3 · see citing works
“This association likely reflects immunosenescence, chronic inflammation, and metabolic dysregulation, which collectively contribute to sarcopenia and functional decline [68-70].”
Deng, Q., Deng, J., Wei, X., Shen, L. H., Chen, J., & Bi, K. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1460811 · Cited by 4 · see citing works
Aghajani, M., Rahmati-Ahmadabad, S., Zamani, F., Ghanbari, B., & Azarbayjani, M. A. (2021) · German Journal of Exercise and Sport Research · doi:10.1007/s12662-021-00749-z · Cited by 3 · see citing works
“IL-6 is affected by factors such as glucocorticoids, catecholamines, insulin, and certain cytokines, such as TNF-α and IL-1, androgens, and thyroid hormones (Straub, 2014; Vicennati, Vottero, Friedman, & Papanicolaou, 2002).”
BackgroundFurgoł, T., Antończyk, R., Miciak, M., et al. (2024) · Polish Journal of Cardio-Thoracic Surgery · doi:10.5114/kitp.2024.138566 · Cited by 2 · see citing works
“Changes in blood hormone levels mainly involve systems responsible for the balance between anabolism and catabolism and an increase in the activity of the renin-angiotensin-aldosterone system [16].”
BackgroundChetina, E. V., Demidova, N. V., & Markova, G. A. (2019) · Modern Rheumatology Journal · doi:10.14412/1996-7012-2019-2-47-54 · Cited by 2 · see citing works
Stress level in companion dogs with and without atopic dermatitis
Park, G.-W., Ataallahi, M., & Park, K.-H. (2024) · Journal of Animal Science and Technology · doi:10.5187/jast.2024.e28 · Cited by 2 · see citing works
“However, when animals are exposed to stimuli over a long period, excessive concentrations of cortisol are produced, which can have detrimental effects [8–10].”
van der Spoel, E., Roelfsema, F., Jansen, S. W. M., Akintola, A. A., Ballieux, B. E. P. B., Cobbaert, C. M., Blauw, G. J., Slagboom, P. E., Westendorp, R. G. J., Pijl, H., et al. (2016) · Frontiers in Endocrinology · doi:10.3389/fendo.2016.00143 · Cited by 2 · see citing works
Dobrovolskaya, O. V., Коваленко, П. С., Toroptsova, N. V., Дыдыкина, И. С., Nikitinskaya, O. A., & Nasonov, E. L. (2019) · Rheumatology Science and Practice · doi:10.14412/1995-4484-2019-160-165 · Cited by 2 · see citing works
“Системный ОП у пациентов с РЗ связывают с хроническим воспалительным процессом и снижением двигательной активности пациентов, а также с приемом пероральных глюкокортикоидов (ГК) [1].”
Heo, J. Y. (2022) · Science Insights · doi:10.15354/si.22.re105 · Cited by 1 · see citing works
“musculoskeletal metabolism and endocrine system, which can directly or indirectly cause debilitation (17, 18).”
BackgroundLarose, C., Samhani, C., Consolandi, P., & Feigerlová, E. (2025) · Endocrine · doi:10.1007/s12020-025-04310-y · Cited by 1 · see citing works
“Low-grade in fl ammation has been recognized as a major patho-physiological mechanism associated with atherosclerosis [15] and with metabolic abnormalities such as metabolic syndrome, obesity or energy storage/expenditure dysregulation [16, 17].”
Farhat, E., Palmisano, M., Marco, M., From, O., Reich, E., Lutz, B., Ramunno, C. F., de Almodóvar, C. R., Bilkei‐Gorzó, A., & Dvir‐Ginzberg, M. (2025) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2025.08.006 · Cited by 1 · see citing works
Ortiz, G. G. R., Granero, R., Icaza, D., & Maraver-Capdevila, L. (2025) · Frontiers in Nutrition · doi:10.3389/fnut.2025.1666688 · Cited by 4 · see citing works
“…to prolonged activation of the hypothalamic–pituitary–adrenal (HPA) axis, which increases the release of the stress hormone cortisol (70, 71) and has thus been associated to a range of adverse physiological effects, including insulin resistance, systemic inflammation, and hormonal imbalance (72).”
Gestational stress disrupts the neuroimmune environment in the nucleus accumbens of maternal rats
Dye, C. N., Franceschelli, D. V., Goodpaster, C. M., Wangler, L. M., Ringland, A., Godbout, J. P., Lenz, K. M., & Leuner, B. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.101140 · Cited by 1 · see citing works
“…characterize the extent to which our model of gestational stress alters endocrine function, as pregnancy and stress elicit complex changes in both neuroinflammatory signaling and hormonal profiles, which could in turn influence one another (Magon and Kumar, 2012; Straub, 2014; Yilmaz et al., 2019).”
Huang, N., & Guan, Y. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2025.1753660 · Cited by 1 · see citing works
“Conversely, cytokines (IFN-γ , IL-6, TNF-α ) modulate hypothalamic–pituitary axes, adipocyte function, and nutrient transporter expression, creating feedback loops that can either amplify or suppress antitumor responses (50, 56).”
Microplastics as drivers of neuroinflammation: a review
Chakrabarti, S. K., & Chattopadhyay, D. (2026) · Journal of Neurology & Stroke · doi:10.15406/jnsk.2026.16.00647 · Cited by 1 · see citing works
Surgical stress: Cortisol and anxiety in surgeons, patients, and stretcher-bearers
Casillas-Cruz, Á. A., Gutiérrez‐García, A. G., & Contreras, C. M. (2019) · Revista de Fomento Social · doi:10.24875/rmn.m19000061 · Cited by 1 · see citing works
Infante, M., Pieri, M., Lupisella, S., Mohamad, A., Bernardini, S., Della‐Morte, D., Fabbri, A., Stefano, A. D., Iannetta, M., Ansaldo, L., et al. (2023) · Current Medical Research and Opinion · doi:10.1080/03007995.2023.2177380 · Cited by 1 · see citing works
- Authors
- Straub, R. H.
- Affiliations
- University Hospital Regensburg (DE)
- Corresponding author
- Straub, Rainer H
- ORCID
- Straub, Rainer H
- Venue
- Arthritis Research & Therapy
- Published
- 2014-02-13
- Volume
- 16
- Issue
- 1
- Pages
- 203-203
- ISSN
- 1478-6354 (ISSN-L)
- 1478-6362
- PMC
- PMC3978663
- OpenAlex
- W2117381377
- Semantic Scholar
- d5bb12b025be69f38e042c0708dff1edebc85d86
- Cited by
- 121
- References
- 150
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 11 · 2023: 8 · 2022: 15 · 2021: 19 · 2020: 6 · 2019: 10 · 2018: 4 · 2017: 6 · 2016: 10 · 2015: 6 · 2014: 7
- FWCI
- 1.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Arthritis Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Keywords
- endocrine-immune interaction, inflammation, energy metabolism, volume regulation, sickness behavior, insulin resistance, insulin-like growth factor I, androgens, vitamin D, osteocalcin, cortisol, norepinephrine, epinephrine, growth hormone, thyroid hormones, angiotensin II, chronic inflammatory diseases, sympathetic nervous system, renin-angiotensin-aldosterone system, vitamin D deficiency, hypercortisolism
- MeSH terms
- Animals, Endocrine System, Energy Metabolism, Humans, Inflammation
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